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2 | 2 | Creatinine Clearance (Cockcroft-Gault Equation) | lab test | decimal | pmc-3597915-1 | Extracted | A 56-year-old man was admitted to the renal unit of the tertiary university hospital with symptoms of polyuria with nocturia, and polydipsia with severe thirst for the past 2 months. Initially, the patient visited a local clinic and was diagnosed as type 2 DM with a fasting blood sugar, 150mg/dL. Despite being controlled hyperglycemia with an oral hypoglycemic agent, he continued drinking daily more than 8 L of cold water (about 10 bottles of refrigerated water, 750 ml capacity) and passed large amounts of urine frequently. He had no specific history including head trauma or mental disorder, and denied any pertinent family history. The patient showed no signs of systemic illness such as fever or arthralgia, or neurologic symptoms involving the central nervous system. He has been working as a gardener with 176 cm in height and 68 kg in weight (71 kg before this event). The physical examination was unremarkable with blood pressure of 132/70 mmHg, pulse rate of 80/min, respiratory rate of 16/min, and temperature of 36.8℃. In the laboratory findings, his white blood cell count was 9,700/mm3; hemoglobin, 13.4 g/dL; platelet, 376×103/mm3; sodium, 140 mEq/L; potassium, 3.8 mEq/L; blood urea nitrogen (BUN), 12 mg/dL; creatinine, 1.0 mg/dL and osmolality 295 mOsm/kg water. HbA1c was 7.2% and post-prandial glucose was checked around 180mg/dl with fasting blood sugar of 140 mg/dL. In urine analysis, the urine pH was 6.0; specific gravity 1.006; albumin (-); glucose (-); WBC 0-4/HPF; RBC 0-2/HPF, and osmolality 140mOsm/kg water. Fluid intake and output in 24 hours recorded 9 L in oral water intake from water containers and 11.7 L in urine output. In hormone assays, ACTH was 25.2 pg/mL (reference value, 6.0-76.0 pg/mL), prolactin 8 µg/L (reference value, 0-15 µg/L), cortisol 9.8 µg/dL (referencel value, 5-25 µg/dL), hGH 2.26 ng/mL (reference value, 0.5-17 ng/mL), and TSH 0.99 µU/mL (reference value, 0.5-4.7 µU/mL). Also, angiotensin converting enzyme (ACE) activity was within normal range (reference value, <40 U/L).
On hospital day 5, the patient underwent a water deprivation test according to the method of Miller-Moses test because of persistent polydipsia and polyuria despite blood glucose control. The results are shown in . During dehydration, the patient lost 3kg (4.4% of body weight), and urine osmolality remained hypotonic below 130 mOsm/kg. Basal ADH level was 5.18 pg/dL, and the repeat ADH level following the stimulation by water deprivation was 3.95 pg/dL, which revealed no increment despite the increased serum osmolality up to 300 mOsm/kg from the baseline levels of 285 to 295 mOsm/kg. One puff (5 µg) of desmopressin nasal spray resulted in the increase of urine osmolality to 266 mOsm/kg (>100% increase from the baseline level, 126 mOsm/kg) and in the marked reduction of urine output from 200-410 ml/hr to 44-60 ml/hr. These results were compatible with CDI,, whose causes would be mostly idiopathic because of normal findings in hypothalamus and hypophysis in magnetic resonance imaging (MRI) scan of sella ().
On discharge (hospital day 9), the dose of desmopressin nasal spray (minirin nasal spray®) was adjusted to 1 puff per 12 hrs (10 µg/day), and urine output was markedly reduced to below 2-3 L/day with no more intense thirst. Also, DM was controlled with fasting blood sugar below 115 mg/dL by metformin (novamet GR® 500mg bid) and American Diabetes Association (ADA) recommended diet. | What is the patient's Creatinine Clearance using the Cockroft-Gault Equation in terms of mL/min? You should use the patient's adjusted body weight in kg instead of the patient's actual body weight if the patient is overweight or obese based on their BMI. If the patient's BMI's normal, set their adjusted body weight to the minimum of the ideal body and actual weight. If the patient is underweight, please set their adjusted body weight to their actual body weight. | {'sex': 'Male', 'age': [56, 'years'], 'weight': [68.0, 'kg'], 'height': [176.0, 'cm'], 'creatinine': [1.0, 'mg/dL']} | 79.333 | 75.366 | 83.3 | The formula for computing Cockcroft-Gault is given by CrCl = ((140 - age) * adjusted weight * (gender_coefficient)) / (serum creatinine * 72), where the gender_coefficient is 1 if male, and 0.85 if female. The serum creatinine concentration is in mg/dL.
The patient's gender is male, which means that the gender coefficient is 1.
The patient is 56 years old.
The concentration of creatinine is 1.0 mg/dL.
The formula for computing the patient's BMI is (weight)/(height * height), where weight is the patient's weight in kg and height is the patient's height in m.
The patient's height is 176.0 cm, which is 176.0 cm * 1 m / 100 cm = 1.76 m. The patient's weight is 68.0 kg. The patient's bmi is therefore 68.0 kg / (1.76 m * 1.76 m) = 21.952 kg/m^2.The patient's BMI is 22.0, indicating they are normal weight.
Because the patient is normal, we take take minimum of the ideal body weight and the patient's body as the patient's adjusted weight for the Cockroft-Gault Equation. Hence, the adjusted body weight is the minimum of the two giving us an adjusted body weight of 68.0 kg.
Using the Cockcroft-Gault equation:
CrCl = ((140 - age) * adjusted weight * gender_coefficient) / (serum creatinine * 72).
Plugging the patient's values gives us ((140 - 56) * 68.0 * 1) / (1.0 * 72) = 79.333 mL/min. Hence, the patient's creatinine clearance is 79.333 mL/min. | A 56-year-old man was admitted to the renal unit of the tertiary university hospital with symptoms of polyuria with nocturia, and polydipsia with severe thirst for the past 2 months. Initially, the patient visited a local clinic and was diagnosed as type 2 DM with a fasting blood sugar, 150mg/dL. Despite being controlled hyperglycemia with an oral hypoglycemic agent, he continued drinking daily more than 8 L of cold water (about 10 bottles of refrigerated water, 750 ml capacity) and passed large amounts of urine frequently. He had no specific history including head trauma or mental disorder, and denied any pertinent family history. The patient showed no signs of systemic illness such as fever or arthralgia, or neurologic symptoms involving the central nervous system. He has been working as a gardener with 176 cm in height and 68 kg in weight (71 kg before this event). The physical examination was unremarkable with blood pressure of 132/70 mmHg, pulse rate of 80/min, respiratory rate of 16/min, and temperature of 36.8℃. In the laboratory findings, his white blood cell count was 9,700/mm3; hemoglobin, 13.4 g/dL; platelet, 376×103/mm3; sodium, 140 mEq/L; potassium, 3.8 mEq/L; blood urea nitrogen (BUN), 12 mg/dL; creatinine, 1.0 mg/dL and osmolality 295 mOsm/kg water. HbA1c was 7.2% and post-prandial glucose was checked around 180mg/dl with fasting blood sugar of 140 mg/dL. In urine analysis, the urine pH was 6.0; specific gravity 1.006; albumin (-); glucose (-); WBC 0-4/HPF; RBC 0-2/HPF, and osmolality 140mOsm/kg water. Fluid intake and output in 24 hours recorded 9 L in oral water intake from water containers and 11.7 L in urine output. In hormone assays, ACTH was 25.2 pg/mL (reference value, 6.0-76.0 pg/mL), prolactin 8 µg/L (reference value, 0-15 µg/L), cortisol 9.8 µg/dL (referencel value, 5-25 µg/dL), hGH 2.26 ng/mL (reference value, 0.5-17 ng/mL), and TSH 0.99 µU/mL (reference value, 0.5-4.7 µU/mL). Also, angiotensin converting enzyme (ACE) activity was within normal range (reference value, <40 U/L).
On hospital day 5, the patient underwent a water deprivation test according to the method of Miller-Moses test because of persistent polydipsia and polyuria despite blood glucose control. The results are shown in . During dehydration, the patient lost 3kg (4.4% of body weight), and urine osmolality remained hypotonic below 130 mOsm/kg. Basal ADH level was 5.18 pg/dL, and the repeat ADH level following the stimulation by water deprivation was 3.95 pg/dL, which revealed no increment despite the increased serum osmolality up to 300 mOsm/kg from the baseline levels of 285 to 295 mOsm/kg. One puff (5 µg) of desmopressin nasal spray resulted in the increase of urine osmolality to 266 mOsm/kg (>100% increase from the baseline level, 126 mOsm/kg) and in the marked reduction of urine output from 200-410 ml/hr to 44-60 ml/hr. These results were compatible with CDI,, whose causes would be mostly idiopathic because of normal findings in hypothalamus and hypophysis in magnetic resonance imaging (MRI) scan of sella ().
On discharge (hospital day 9), the dose of desmopressin nasal spray (minirin nasal spray®) was adjusted to 1 puff per 12 hrs (10 µg/day), and urine output was markedly reduced to below 2-3 L/day with no more intense thirst. Also, DM was controlled with fasting blood sugar below 115 mg/dL by metformin (novamet GR® 500mg bid) and American Diabetes Association (ADA) recommended diet.
What is the patient's Creatinine Clearance using the Cockroft-Gault Equation in terms of mL/min? You should use the patient's adjusted body weight in kg instead of the patient's actual body weight if the patient is overweight or obese based on their BMI. If the patient's BMI's normal, set their adjusted body weight to the minimum of the ideal body and actual weight. If the patient is underweight, please set their adjusted body weight to their actual body weight.
Creatinine Clearance (Cockcroft-Gault Equation): CrCl = ((140 - age) * adjusted weight * (gender_coefficient)) / (serum creatinine * 72), where the gender_coefficient is 1 if male, and 0.85 if female | |
3 | 2 | Creatinine Clearance (Cockcroft-Gault Equation) | lab test | decimal | pmc-7737526-1 | Extracted | In 2008, a 59-year-old Japanese woman was admitted for evaluation of renal disease. RA had been diagnosed at another hospital in 1972 when she presented with bilateral arthropathy of the hands, knees, ankles, and feet. Treatment was started with a combination of a gold preparation and nonsteroidal anti-inflammatory drugs (NSAIDs), but was not been effective. Prednisolone (PSL; 15 mg daily) and bucillamine (BUC; 200 mg daily) were started in 1987, but her disease remained active. Methotrexate (MTX; 5 mg daily) was started in 1995 but was discontinued because of nausea. In 2002, urinary protein was found to be positive by a dipstick urine test, and BUC was stopped. Then treatment was continued with PSL (5 mg/day) and loxoprofen (50 mg/day). However, urinary protein excretion increased in 2007, and serum creatinine (Cre) was elevated to 1.96 mg/dL.
On admission, the patient was 154.2 cm tall and weighed 44.0 kg, with a blood pressure of 128/60 mmHg and temperature of 36.4 °C. Physical examination did not reveal any abnormalities of the heart and lungs. The joints of her hands, knees, ankles, and feet showed bilateral swelling and deformity. In addition, the lower extremities were edematous. Her cervical spine was unstable, with flexion causing numbness in the upper limbs.
Laboratory findings were as follows: serum Cre was 4.2 mg/dL, the estimated glomerular filtration rate (eGFR) was 9.3 mL/min/1.73m3, C-reactive protein (CRP) was 0.9 mg/dL, and SAA was 43.2. In addition, rheumatoid factor (RF) was positive at 59 U/mL (normal: < 10), and cyclic citrullinated peptide (CCP) antibodies were positive at 218.5 (normal < 4.5). 24-hour urinary protein excretion was 6.5 g, and the urine sediment contained 1 – 5 red cells per high-power field (HPF). The disease activity score (DAS)-CRP was 7.1. Radiographs showed deformation of the finger and foot joints as well as atlantoaxial joint subluxation. Renal biopsy was performed for evaluation of her kidney disease.
Renal biopsy
Light microscopic examination of a biopsy specimen containing 4 glomeruli revealed global sclerosis in all 4. There was severe tubular atrophy, and tubulointerstitial fibrosis occupied ~ 95% of the entire renal cortex. All 4 glomeruli contained multinodular structures of amorphous material with a PAM-positive border. This material was positive for Congo-red and amyloid A, but was negative for κ and λ chains, β-2 microglobulin, and transthyretin (). Electron microscopy showed randomly arranged fibrils measuring 8 – 12 nm in diameter corresponding to the amyloid deposits (f). AA amyloidosis was diagnosed from these findings. In addition to the glomeruli, amyloid deposits were mainly observed in the interlobular artery walls and tubulointerstitium (e). Endoscopic biopsy of the stomach, duodenum, and colon revealed AA-positive deposits in the small arteries and tissues of the submucosal layer (a).
Clinical course
PSL was discontinued, and administration of a soluble tumor necrosis factor (TNF) receptor inhibitor (etanercept; 25 mg every 2 weeks) was started in May 2008, but it was not effective. By September 2008, Cre was increased to 6.0 mg/dL. She underwent surgery to prepare an arteriovenous fistula for hemodialysis. Etanercept was discontinued, and a humanized anti-interleukin-6 receptor antibody (tocilizumab; 8 mg/kg = 360 mg/month) was started in February 2009. After 3 months, her CRP decreased to 0.0 mg/dL, and the DAS28-CRP sore was 2.12. After 2 years of tocilizumab therapy, urinary protein excretion was decreased to 1.1 g/day, and Cre was 4.0 mg/dL. Subsequently, Cre remained in the range of 4.5 – 5.0 mg/dL until December 2017. While Cre increased to 7.1 mg/dL after initiation of treatment with denosumab (a human monoclonal antibody that binds to receptor activator of NFκB ligand) for osteoporosis in October 2018, it remained at 7.0 mg/dL in June 2019 ().
Gastroduodenal biopsy was performed in May 2013 and May 2017. On both occasions, no amyloid deposits were detected in the submucosal blood vessels (b). | What is the patient's Creatinine Clearance using the Cockroft-Gault Equation in terms of mL/min? You should use the patient's adjusted body weight in kg instead of the patient's actual body weight if the patient is overweight or obese based on their BMI. If the patient's BMI's normal, set their adjusted body weight to the minimum of the ideal body and actual weight. If the patient is underweight, please set their adjusted body weight to their actual body weight. | {'sex': 'Female', 'age': [59, 'years'], 'weight': [44.0, 'kg'], 'height': [154.2, 'cm'], 'creatinine': [1.96, 'mg/dL']} | 21.467 | 20.394 | 22.54 | The formula for computing Cockcroft-Gault is given by CrCl = ((140 - age) * adjusted weight * (gender_coefficient)) / (serum creatinine * 72), where the gender_coefficient is 1 if male, and 0.85 if female. The serum creatinine concentration is in mg/dL.
The patient's gender is female, which means that the gender coefficient is 0.85.
The patient is 59 years old.
The concentration of creatinine is 1.96 mg/dL.
The formula for computing the patient's BMI is (weight)/(height * height), where weight is the patient's weight in kg and height is the patient's height in m.
The patient's height is 154.2 cm, which is 154.2 cm * 1 m / 100 cm = 1.542 m. The patient's weight is 44.0 kg. The patient's bmi is therefore 44.0 kg / (1.542 m * 1.542 m) = 18.505 kg/m^2.The patient's BMI is 18.5, indicating they are normal weight.
Because the patient is normal, we take take minimum of the ideal body weight and the patient's body as the patient's adjusted weight for the Cockroft-Gault Equation. Hence, the adjusted body weight is the minimum of the two giving us an adjusted body weight of 44.0 kg.
Using the Cockcroft-Gault equation:
CrCl = ((140 - age) * adjusted weight * gender_coefficient) / (serum creatinine * 72).
Plugging the patient's values gives us ((140 - 59) * 44.0 * 0.85) / (1.96 * 72) = 21.467 mL/min. Hence, the patient's creatinine clearance is 21.467 mL/min. | In 2008, a 59-year-old Japanese woman was admitted for evaluation of renal disease. RA had been diagnosed at another hospital in 1972 when she presented with bilateral arthropathy of the hands, knees, ankles, and feet. Treatment was started with a combination of a gold preparation and nonsteroidal anti-inflammatory drugs (NSAIDs), but was not been effective. Prednisolone (PSL; 15 mg daily) and bucillamine (BUC; 200 mg daily) were started in 1987, but her disease remained active. Methotrexate (MTX; 5 mg daily) was started in 1995 but was discontinued because of nausea. In 2002, urinary protein was found to be positive by a dipstick urine test, and BUC was stopped. Then treatment was continued with PSL (5 mg/day) and loxoprofen (50 mg/day). However, urinary protein excretion increased in 2007, and serum creatinine (Cre) was elevated to 1.96 mg/dL.
On admission, the patient was 154.2 cm tall and weighed 44.0 kg, with a blood pressure of 128/60 mmHg and temperature of 36.4 °C. Physical examination did not reveal any abnormalities of the heart and lungs. The joints of her hands, knees, ankles, and feet showed bilateral swelling and deformity. In addition, the lower extremities were edematous. Her cervical spine was unstable, with flexion causing numbness in the upper limbs.
Laboratory findings were as follows: serum Cre was 4.2 mg/dL, the estimated glomerular filtration rate (eGFR) was 9.3 mL/min/1.73m3, C-reactive protein (CRP) was 0.9 mg/dL, and SAA was 43.2. In addition, rheumatoid factor (RF) was positive at 59 U/mL (normal: < 10), and cyclic citrullinated peptide (CCP) antibodies were positive at 218.5 (normal < 4.5). 24-hour urinary protein excretion was 6.5 g, and the urine sediment contained 1 – 5 red cells per high-power field (HPF). The disease activity score (DAS)-CRP was 7.1. Radiographs showed deformation of the finger and foot joints as well as atlantoaxial joint subluxation. Renal biopsy was performed for evaluation of her kidney disease.
Renal biopsy
Light microscopic examination of a biopsy specimen containing 4 glomeruli revealed global sclerosis in all 4. There was severe tubular atrophy, and tubulointerstitial fibrosis occupied ~ 95% of the entire renal cortex. All 4 glomeruli contained multinodular structures of amorphous material with a PAM-positive border. This material was positive for Congo-red and amyloid A, but was negative for κ and λ chains, β-2 microglobulin, and transthyretin (). Electron microscopy showed randomly arranged fibrils measuring 8 – 12 nm in diameter corresponding to the amyloid deposits (f). AA amyloidosis was diagnosed from these findings. In addition to the glomeruli, amyloid deposits were mainly observed in the interlobular artery walls and tubulointerstitium (e). Endoscopic biopsy of the stomach, duodenum, and colon revealed AA-positive deposits in the small arteries and tissues of the submucosal layer (a).
Clinical course
PSL was discontinued, and administration of a soluble tumor necrosis factor (TNF) receptor inhibitor (etanercept; 25 mg every 2 weeks) was started in May 2008, but it was not effective. By September 2008, Cre was increased to 6.0 mg/dL. She underwent surgery to prepare an arteriovenous fistula for hemodialysis. Etanercept was discontinued, and a humanized anti-interleukin-6 receptor antibody (tocilizumab; 8 mg/kg = 360 mg/month) was started in February 2009. After 3 months, her CRP decreased to 0.0 mg/dL, and the DAS28-CRP sore was 2.12. After 2 years of tocilizumab therapy, urinary protein excretion was decreased to 1.1 g/day, and Cre was 4.0 mg/dL. Subsequently, Cre remained in the range of 4.5 – 5.0 mg/dL until December 2017. While Cre increased to 7.1 mg/dL after initiation of treatment with denosumab (a human monoclonal antibody that binds to receptor activator of NFκB ligand) for osteoporosis in October 2018, it remained at 7.0 mg/dL in June 2019 ().
Gastroduodenal biopsy was performed in May 2013 and May 2017. On both occasions, no amyloid deposits were detected in the submucosal blood vessels (b).
What is the patient's Creatinine Clearance using the Cockroft-Gault Equation in terms of mL/min? You should use the patient's adjusted body weight in kg instead of the patient's actual body weight if the patient is overweight or obese based on their BMI. If the patient's BMI's normal, set their adjusted body weight to the minimum of the ideal body and actual weight. If the patient is underweight, please set their adjusted body weight to their actual body weight.
Creatinine Clearance (Cockcroft-Gault Equation): CrCl = ((140 - age) * adjusted weight * (gender_coefficient)) / (serum creatinine * 72), where the gender_coefficient is 1 if male, and 0.85 if female | |
4 | 2 | Creatinine Clearance (Cockcroft-Gault Equation) | lab test | decimal | pmc-2813128-1 | Extracted | A 34-year-old man was admitted for evaluation of worsening pedal edema. He was apparently healthy until four years back, when he developed edema of both feet and nonpruritic macular skin rash involving both lower limbs. Subsequently, he was detected to have hypertension, proteinuria and mild renal failure (6 months ago). He had no history of arthralgia, Raynaud's phenomenon, paraesthesia or gastrointestinal hemorrhage.
Six weeks prior to admission in our centre, he developed weakness of left upper and lower limbs with slurring of speech and was hospitalized elsewhere. A computerized tomographic scan of head had revealed an infarct in the right middle cerebral artery territory and he was treated with aspirin, statins, and antihypertensives. He made a complete recovery but was detected to have renal failure and was referred to us for further evaluation.
He weighed 74 kg and had a height of 174 cm. He had pallor and bilateral pitting pedal edema. There was no skin rash or lymphadenopathy. Blood pressure was 140/90 mmHg. Examination of cardiovascular system, respiratory system, and abdomen was normal. There were no neurological deficits.
Investigations revealed hemoglobin of 8.79 gm/dL, platelet count of 112000/mm3, total WBC count of 7960/mm3 - with a normal differential count, ESR of 40 mm at end of first hour. Urinalysis showed protein ++++, 6-8 RBCs/HPF; and 24 hour urine protein was 4420 mg. Blood urea was 72 mg/dL and serum creatinine was 3.1 mg/dL with normal serum levels of electrolytes. Liver function tests, PT and aPTT were normal. Serum albumin was 3.6 gm%, serum globulin 3.8 g/dL and serum cholesterol 240 mg/dL. Serum protein electrophoresis was normal. Blood and urine cultures were sterile. HBsAg, antihepatitis C virus (HCV) and HIV antibodies were negative VDRL, cANCA, pANCA, antiphospholipid antibodies, ANA, antids DNA were negative. Serum homocysteine [12 µmol/L] was normal and serum complement levels were reduced (C3:70 mg/dL, C4:18 mg/dL). Serum cryoglobulin assay was positive. On PAGE electrophoresis, the mobility was suggestive of mixed cryoglobulins. HCV RNA was negative in serum [polymerase chain reaction (PCR)]. Qualitative analysis for HCV RNA [by reverse transcriptase-PCR (RT-PCR)] in the cryoprecipitate was negative []. Doppler study of extra cranial carotid and vertebral vessels was normal. Ultra sonogram of abdomen, ECG, and echocardiogram were normal. Bone marrow examination was normal. X-rays of chest, skull spine, and pelvis were normal. Kidney biopsy showed lobular accentuation of glomeruli with mesangial proliferation, mild endocapillary proliferation, and double contour of glomerular basement membrane on light microscopy. Intracapillary eosinophilic PAS positive hyaline deposits were noted []. Interstitium showed mononuclear infiltrates. Immunofluorescence showed mesangial and capillary granular positivity for C3 IgG and IgM. | What is the patient's Creatinine Clearance using the Cockroft-Gault Equation in terms of mL/min? You should use the patient's adjusted body weight in kg instead of the patient's actual body weight if the patient is overweight or obese based on their BMI. If the patient's BMI's normal, set their adjusted body weight to the minimum of the ideal body and actual weight. If the patient is underweight, please set their adjusted body weight to their actual body weight. | {'sex': 'Male', 'age': [34, 'years'], 'weight': [74.0, 'kg'], 'height': [174.0, 'cm'], 'creatinine': [3.1, 'mg/dL']} | 33.034 | 31.382 | 34.686 | The formula for computing Cockcroft-Gault is given by CrCl = ((140 - age) * adjusted weight * (gender_coefficient)) / (serum creatinine * 72), where the gender_coefficient is 1 if male, and 0.85 if female. The serum creatinine concentration is in mg/dL.
The patient's gender is male, which means that the gender coefficient is 1.
The patient is 34 years old.
The concentration of creatinine is 3.1 mg/dL.
The formula for computing the patient's BMI is (weight)/(height * height), where weight is the patient's weight in kg and height is the patient's height in m.
The patient's height is 174.0 cm, which is 174.0 cm * 1 m / 100 cm = 1.74 m. The patient's weight is 74.0 kg. The patient's bmi is therefore 74.0 kg / (1.74 m * 1.74 m) = 24.442 kg/m^2.The patient's BMI is 24.4, indicating they are normal weight.
Because the patient is normal, we take take minimum of the ideal body weight and the patient's body as the patient's adjusted weight for the Cockroft-Gault Equation. Hence, the adjusted body weight is the minimum of the two giving us an adjusted body weight of 69.559 kg.
Using the Cockcroft-Gault equation:
CrCl = ((140 - age) * adjusted weight * gender_coefficient) / (serum creatinine * 72).
Plugging the patient's values gives us ((140 - 34) * 69.559 * 1) / (3.1 * 72) = 33.034 mL/min. Hence, the patient's creatinine clearance is 33.034 mL/min. | A 34-year-old man was admitted for evaluation of worsening pedal edema. He was apparently healthy until four years back, when he developed edema of both feet and nonpruritic macular skin rash involving both lower limbs. Subsequently, he was detected to have hypertension, proteinuria and mild renal failure (6 months ago). He had no history of arthralgia, Raynaud's phenomenon, paraesthesia or gastrointestinal hemorrhage.
Six weeks prior to admission in our centre, he developed weakness of left upper and lower limbs with slurring of speech and was hospitalized elsewhere. A computerized tomographic scan of head had revealed an infarct in the right middle cerebral artery territory and he was treated with aspirin, statins, and antihypertensives. He made a complete recovery but was detected to have renal failure and was referred to us for further evaluation.
He weighed 74 kg and had a height of 174 cm. He had pallor and bilateral pitting pedal edema. There was no skin rash or lymphadenopathy. Blood pressure was 140/90 mmHg. Examination of cardiovascular system, respiratory system, and abdomen was normal. There were no neurological deficits.
Investigations revealed hemoglobin of 8.79 gm/dL, platelet count of 112000/mm3, total WBC count of 7960/mm3 - with a normal differential count, ESR of 40 mm at end of first hour. Urinalysis showed protein ++++, 6-8 RBCs/HPF; and 24 hour urine protein was 4420 mg. Blood urea was 72 mg/dL and serum creatinine was 3.1 mg/dL with normal serum levels of electrolytes. Liver function tests, PT and aPTT were normal. Serum albumin was 3.6 gm%, serum globulin 3.8 g/dL and serum cholesterol 240 mg/dL. Serum protein electrophoresis was normal. Blood and urine cultures were sterile. HBsAg, antihepatitis C virus (HCV) and HIV antibodies were negative VDRL, cANCA, pANCA, antiphospholipid antibodies, ANA, antids DNA were negative. Serum homocysteine [12 µmol/L] was normal and serum complement levels were reduced (C3:70 mg/dL, C4:18 mg/dL). Serum cryoglobulin assay was positive. On PAGE electrophoresis, the mobility was suggestive of mixed cryoglobulins. HCV RNA was negative in serum [polymerase chain reaction (PCR)]. Qualitative analysis for HCV RNA [by reverse transcriptase-PCR (RT-PCR)] in the cryoprecipitate was negative []. Doppler study of extra cranial carotid and vertebral vessels was normal. Ultra sonogram of abdomen, ECG, and echocardiogram were normal. Bone marrow examination was normal. X-rays of chest, skull spine, and pelvis were normal. Kidney biopsy showed lobular accentuation of glomeruli with mesangial proliferation, mild endocapillary proliferation, and double contour of glomerular basement membrane on light microscopy. Intracapillary eosinophilic PAS positive hyaline deposits were noted []. Interstitium showed mononuclear infiltrates. Immunofluorescence showed mesangial and capillary granular positivity for C3 IgG and IgM.
What is the patient's Creatinine Clearance using the Cockroft-Gault Equation in terms of mL/min? You should use the patient's adjusted body weight in kg instead of the patient's actual body weight if the patient is overweight or obese based on their BMI. If the patient's BMI's normal, set their adjusted body weight to the minimum of the ideal body and actual weight. If the patient is underweight, please set their adjusted body weight to their actual body weight.
Creatinine Clearance (Cockcroft-Gault Equation): CrCl = ((140 - age) * adjusted weight * (gender_coefficient)) / (serum creatinine * 72), where the gender_coefficient is 1 if male, and 0.85 if female | |
5 | 2 | Creatinine Clearance (Cockcroft-Gault Equation) | lab test | decimal | pmc-5544981-1 | Extracted | A 67-year-old Japanese woman underwent OWHTO to treat SPONK that had occurred in the left medial femoral condyle (Fig. ). The patient reported the following history of the present illness. Pain in the left knee joint initially occurred at 1 year and 4 months before admission, without any particular trigger. Her former treating physician had provided conservative treatments such as oral administration of anti-inflammatory analgesics, rehabilitation including quadriceps muscle training, and guidance on the use of a cane to relieve weight bearing. However, this treatment was not successful in relieving her symptoms, and she was referred to our department for surgery. The patient had a history of hypertension and hyperlipidemia, and she had been taking oral candesartan and atorvastatin. The patient was a housewife with no noteworthy aspects related to social, family, or environmental history. On physical examination, the patient had a height of 157 cm, a body weight of 62 kg, and a body mass index of 25.2 kg/m2. She reported feeling pain in the medial joint space of the knee during walking, as well as during climbing or descending stairs. At the time of the first admission, her systolic/diastolic blood pressure was 165/97 mmHg. Table provides an overview of the patient’s pain scores in the knee joint, ROM of the knee joint, and knee joint function. Neurological examination revealed no abnormal findings. Similarly, laboratory findings at the time of the first admission did not indicate any abnormality: total protein 7.3 g/dl, albumin 4.6 g/dl, aspartate aminotransferase 22 U/L, alanine aminotransferase 18 U/L, lactate dehydrogenase 213 U/L, alkaline phosphatase 297 U/L, γ-glutamyl transferase 18 U/L, total bilirubin 0.6 mg/dl, Na 142 mEq/L, Cl 104 mEq/L, K 4.5 mEq/L, blood urea nitrogen 21.4 mg/dl, creatinine 0.56 mg/dl, Ca 9.7 mg/dl, inorganic phosphorus 3.7 mg/dl, leukocytes 5100/μl, erythrocytes 5.00 × 106/μl, hemoglobin 14.4 g/dl, hematocrit 43.6%, and platelets 263 × 103/μl.
The HAL-SJ treatment program was divided into five phases []. Phase 1 consisted of preoperative observation from the day of hospital admission until the day of surgery. The patient’s thigh circumference and lower leg length were measured preoperatively to adjust the HAL-SJ to the patient’s physical size, which would ensure appropriate training. We palpated the patient’s quadriceps muscles (vastus medialis, rectus femoris, and vastus lateralis) and attached electrodes to each muscle to detect the bioelectric potentials of the long axis along the belly of each muscle. We instructed the patient to perform knee extension and to contract her quadriceps. On the basis of these data, we instructed the patient to simulate the knee extension training, which would be performed postoperatively. Specifically, the patient sat with her lower leg hanging down naturally, and the height of the chair was adjusted so that the patient’s feet were not in contact with the floor. The patient performed ten knee extensions with HAL-SJ assistance, using the muscle that exhibited the largest bioelectric potential amplitude.
Phase 2 involved surgery (day of surgery). The patient underwent OWHTO (Figs. and ) using TomoFix (DePuy Synthes, Bettlach, Switzerland), artificial bone (OSferion60, β-tricalcium phosphate; Olympus Terumo Biomaterials, Tokyo, Japan), and biplanar osteotomy, as described by Takeuchi et al. []. The preoperative weight-bearing line (WBL) percentage [], calculated on the basis of an anteroposterior weight-bearing radiograph of the affected leg in full knee extension, was 29.6%. The surgery was planned with a target postoperative WBL percentage of 62.5%. The actual enlarged angle and distance of osteotomy were 5.5 degrees and 7 mm, respectively.
Phase 3 consisted of postoperative observation from day 1 to day 7 postoperatively. For postoperative rehabilitation, partial weight bearing was allowed after a non-weight-bearing period of 2 weeks, and full weight bearing began at 4 weeks postoperatively. The patient received rehabilitation training under the guidance of a physical therapist (ROM exercises and muscle-strengthening training) for 20–40 minutes each day, 5 days per week, from the first postoperative day until discharge. For ROM exercises, continuous passive motion training began on the first postoperative day for 1 hour per day and continued every day until discharge. On postoperative day 7, we attached electrodes to the quadriceps muscle to detect the bioelectric potential along the long axis of the rectus femoris muscle belly (Fig. ). Then, the patient was instructed to perform active knee extension exercises that involved contracting her quadriceps, thus simulating training with HAL-SJ (Fig. ).
Phase 4 consisted of HAL-SJ therapy from postoperative day 8 to discharge. The CVC mode of HAL-SJ serves to support the patient’s voluntary motion on the basis of voluntary muscle activity and the assistive torque provided to the knee joint []. In this study, we used the CVC mode, which allowed the operator to adjust the degree of physical support to maintain the patient’s comfort while gradually reducing support as training progressed. In addition to the regular rehabilitation program (Fig. ), the patient performed HAL-JS-assisted knee extension exercises while sitting, which consisted of five sets of ten repetitions per set, twice per week (Fig. ). The training was performed six times before the patient was discharged (postoperative days 8, 10, 15, 17, 22, and 24). The mean training duration, including the time required to put on the HAL-SJ, was 15.5 ± 1.4 minutes (15 minutes, 16 minutes, 17 minutes, 16 minutes, 13 minutes, and 16 minutes during training sessions 1, 2, 3, 4, 5, and 6, respectively). There were no adverse events related to the use of HAL-SJ, and the patient was discharged 30 days after the surgery.
Phase 5 consisted of post-HAL-SJ therapy observation from discharge until 3 months after the end of HAL-SJ therapy, during which the following indicators were assessed: EL, assessed as the difference between the maximum knee joint extension angle during passive exercise and that during active exercise; knee pain rated on the visual analogue scale (VAS); isometric knee extension muscle strength (IKEMS); active ROM before surgery, before and after HAL-SJ training, and at 1 and 3 months after the end of training; and the Japanese Orthopaedic Association (JOA) score [] before surgery, at discharge, and at 1 and 3 months after the end of training. Furthermore, we used lateral radiographs to measure the tibial slope angle (TSA) and Insall-Salvati ratio (ISR) as indicators of patellar tendon shortening before surgery and after implant removal at 1 year after the operation [] (Fig. ). Measurement of knee ROM was performed using goniometry, and the landmarks used in the measurements were the greater trochanter of the femur, proximal head of the fibula, and lateral malleolus. Goniometry was used because it has been reported that goniometric measurements of ROM are more reliable than visual observation, with an accuracy of up to 1.0 degree []. The maximal IKEMS of the operated leg was assessed with the patient in a sitting position, with the hips and knees flexed at 90 degrees. A μTas F-1 handheld dynamometer (Anima Corp., Tokyo, Japan) was fixed to the chair, and two measurements were recorded. Each trial lasted 3–5 seconds, with 30 seconds of rest between trials. The higher score of two valid trials was recorded. All measurements were performed by a single trained physical therapist to eliminate interobserver variability. The EL, VAS, IKEMS, and ROM results are shown in Table . The EL improved from 3 degrees preoperatively to 0 degrees at the end of the sixth HAL-SJ training session, but it returned to 3 degrees at 1 and 3 months after the end of the training. When we compared results obtained before training against those obtained after each of the six training sessions, we observed that three sessions produced improved EL and three sessions produced improved or relatively constant VAS scores immediately after training. However, for the other three sessions, the patient reported increased pain immediately after training, with the greatest increase in pain reported immediately after the first HAL-SJ training session, when the VAS score was 1.7 times higher immediately after training than before training. The EL improved after training sessions 1 and 3, when the patient reported increased knee pain (expressed as the VAS score). However, the EL did not change after training sessions 2 and 4, when the patient reported less knee pain (improved VAS score immediately after training). The patient did not refuse to undergo training because of increased pain. The IKEMS value was the largest preoperatively (17.6 kgf) and decreased to its lowest value (30% of the preoperative strength) before the first HAL-SJ intervention at 8 days after the operation. The IKEMS remained relatively constant throughout HAL-SJ training but recovered to the preoperative value during follow-up (18.7 and 16.6 kgf at 1 and 3 months, respectively, after completion of HAL-SJ training). The active ROM also recovered to the preoperative value by the end of the sixth HAL-SJ training session. Thereafter, the extension ROM did not change, but the flexion ROM was maintained or improved. The JOA score decreased from 60 points preoperatively to 55 points at discharge, but it improved with time, reaching 65 and 85 points at 1 and 3 months, respectively, after the end of HAL-SJ training. Whereas the TSA was maintained at 13.1 degrees before and after the surgery, the ISR decreased from 1.13 preoperatively to 0.97 postoperatively. At 6 months after surgery, the passive ROM was 0–135 degrees, and the JOA score was 90 points. There were no complications throughout the preparation, surgery, or rehabilitation process. | What is the patient's Creatinine Clearance using the Cockroft-Gault Equation in terms of mL/min? You should use the patient's adjusted body weight in kg instead of the patient's actual body weight if the patient is overweight or obese based on their BMI. If the patient's BMI's normal, set their adjusted body weight to the minimum of the ideal body and actual weight. If the patient is underweight, please set their adjusted body weight to their actual body weight. | {'sex': 'Female', 'weight': [62.0, 'kg'], 'height': [157.0, 'cm'], 'creatinine': [0.56, 'mg/dL'], 'age': [67, 'years']} | 84.025 | 79.824 | 88.226 | The formula for computing Cockcroft-Gault is given by CrCl = ((140 - age) * adjusted weight * (gender_coefficient)) / (serum creatinine * 72), where the gender_coefficient is 1 if male, and 0.85 if female. The serum creatinine concentration is in mg/dL.
The patient's gender is female, which means that the gender coefficient is 0.85.
The patient is 67 years old.
The concentration of creatinine is 0.56 mg/dL.
The formula for computing the patient's BMI is (weight)/(height * height), where weight is the patient's weight in kg and height is the patient's height in m.
The patient's height is 157.0 cm, which is 157.0 cm * 1 m / 100 cm = 1.57 m. The patient's weight is 62.0 kg. The patient's bmi is therefore 62.0 kg / (1.57 m * 1.57 m) = 25.153 kg/m^2.The patient's BMI is 25.2, indicating they are overweight/obese.
Because the patient is overweight/obese, we use the adjusted body weight formula to get the adjusted weight used for Cockroft-Gault Equation. Shown below is the computation for IBW (ideal body weight).
The patient's gender is Female.
The patient's height is 157.0 cm, which is 157.0 cm * 0.393701 in/cm = 61.811 in.
For females, the ideal body weight (IBW) is calculated as follows:
IBW = 45.5 kg + 2.3 kg * (height (in inches) - 60)
Plugging in the values gives us 45.5 kg + 2.3 kg * (61.811 (in inches) - 60) = 49.665 kg.
Hence, the patient's IBW is 49.665 kg.Shown below is the computation for ABW (adjusted body weight).
To compute the ABW value, apply the following formula: ABW = IBW + 0.4 * (weight (in kg) - IBW (in kg)). ABW = 49.665 kg + 0.4 * (62.0 kg - 49.665 kg) = 54.599 kg. The patient's adjusted body weight is 54.599 kg.
Using the Cockcroft-Gault equation:
CrCl = ((140 - age) * adjusted weight * gender_coefficient) / (serum creatinine * 72).
Plugging the patient's values gives us ((140 - 67) * 54.599 * 0.85) / (0.56 * 72) = 84.025 mL/min. Hence, the patient's creatinine clearance is 84.025 mL/min. | A 67-year-old Japanese woman underwent OWHTO to treat SPONK that had occurred in the left medial femoral condyle (Fig. ). The patient reported the following history of the present illness. Pain in the left knee joint initially occurred at 1 year and 4 months before admission, without any particular trigger. Her former treating physician had provided conservative treatments such as oral administration of anti-inflammatory analgesics, rehabilitation including quadriceps muscle training, and guidance on the use of a cane to relieve weight bearing. However, this treatment was not successful in relieving her symptoms, and she was referred to our department for surgery. The patient had a history of hypertension and hyperlipidemia, and she had been taking oral candesartan and atorvastatin. The patient was a housewife with no noteworthy aspects related to social, family, or environmental history. On physical examination, the patient had a height of 157 cm, a body weight of 62 kg, and a body mass index of 25.2 kg/m2. She reported feeling pain in the medial joint space of the knee during walking, as well as during climbing or descending stairs. At the time of the first admission, her systolic/diastolic blood pressure was 165/97 mmHg. Table provides an overview of the patient’s pain scores in the knee joint, ROM of the knee joint, and knee joint function. Neurological examination revealed no abnormal findings. Similarly, laboratory findings at the time of the first admission did not indicate any abnormality: total protein 7.3 g/dl, albumin 4.6 g/dl, aspartate aminotransferase 22 U/L, alanine aminotransferase 18 U/L, lactate dehydrogenase 213 U/L, alkaline phosphatase 297 U/L, γ-glutamyl transferase 18 U/L, total bilirubin 0.6 mg/dl, Na 142 mEq/L, Cl 104 mEq/L, K 4.5 mEq/L, blood urea nitrogen 21.4 mg/dl, creatinine 0.56 mg/dl, Ca 9.7 mg/dl, inorganic phosphorus 3.7 mg/dl, leukocytes 5100/μl, erythrocytes 5.00 × 106/μl, hemoglobin 14.4 g/dl, hematocrit 43.6%, and platelets 263 × 103/μl.
The HAL-SJ treatment program was divided into five phases []. Phase 1 consisted of preoperative observation from the day of hospital admission until the day of surgery. The patient’s thigh circumference and lower leg length were measured preoperatively to adjust the HAL-SJ to the patient’s physical size, which would ensure appropriate training. We palpated the patient’s quadriceps muscles (vastus medialis, rectus femoris, and vastus lateralis) and attached electrodes to each muscle to detect the bioelectric potentials of the long axis along the belly of each muscle. We instructed the patient to perform knee extension and to contract her quadriceps. On the basis of these data, we instructed the patient to simulate the knee extension training, which would be performed postoperatively. Specifically, the patient sat with her lower leg hanging down naturally, and the height of the chair was adjusted so that the patient’s feet were not in contact with the floor. The patient performed ten knee extensions with HAL-SJ assistance, using the muscle that exhibited the largest bioelectric potential amplitude.
Phase 2 involved surgery (day of surgery). The patient underwent OWHTO (Figs. and ) using TomoFix (DePuy Synthes, Bettlach, Switzerland), artificial bone (OSferion60, β-tricalcium phosphate; Olympus Terumo Biomaterials, Tokyo, Japan), and biplanar osteotomy, as described by Takeuchi et al. []. The preoperative weight-bearing line (WBL) percentage [], calculated on the basis of an anteroposterior weight-bearing radiograph of the affected leg in full knee extension, was 29.6%. The surgery was planned with a target postoperative WBL percentage of 62.5%. The actual enlarged angle and distance of osteotomy were 5.5 degrees and 7 mm, respectively.
Phase 3 consisted of postoperative observation from day 1 to day 7 postoperatively. For postoperative rehabilitation, partial weight bearing was allowed after a non-weight-bearing period of 2 weeks, and full weight bearing began at 4 weeks postoperatively. The patient received rehabilitation training under the guidance of a physical therapist (ROM exercises and muscle-strengthening training) for 20–40 minutes each day, 5 days per week, from the first postoperative day until discharge. For ROM exercises, continuous passive motion training began on the first postoperative day for 1 hour per day and continued every day until discharge. On postoperative day 7, we attached electrodes to the quadriceps muscle to detect the bioelectric potential along the long axis of the rectus femoris muscle belly (Fig. ). Then, the patient was instructed to perform active knee extension exercises that involved contracting her quadriceps, thus simulating training with HAL-SJ (Fig. ).
Phase 4 consisted of HAL-SJ therapy from postoperative day 8 to discharge. The CVC mode of HAL-SJ serves to support the patient’s voluntary motion on the basis of voluntary muscle activity and the assistive torque provided to the knee joint []. In this study, we used the CVC mode, which allowed the operator to adjust the degree of physical support to maintain the patient’s comfort while gradually reducing support as training progressed. In addition to the regular rehabilitation program (Fig. ), the patient performed HAL-JS-assisted knee extension exercises while sitting, which consisted of five sets of ten repetitions per set, twice per week (Fig. ). The training was performed six times before the patient was discharged (postoperative days 8, 10, 15, 17, 22, and 24). The mean training duration, including the time required to put on the HAL-SJ, was 15.5 ± 1.4 minutes (15 minutes, 16 minutes, 17 minutes, 16 minutes, 13 minutes, and 16 minutes during training sessions 1, 2, 3, 4, 5, and 6, respectively). There were no adverse events related to the use of HAL-SJ, and the patient was discharged 30 days after the surgery.
Phase 5 consisted of post-HAL-SJ therapy observation from discharge until 3 months after the end of HAL-SJ therapy, during which the following indicators were assessed: EL, assessed as the difference between the maximum knee joint extension angle during passive exercise and that during active exercise; knee pain rated on the visual analogue scale (VAS); isometric knee extension muscle strength (IKEMS); active ROM before surgery, before and after HAL-SJ training, and at 1 and 3 months after the end of training; and the Japanese Orthopaedic Association (JOA) score [] before surgery, at discharge, and at 1 and 3 months after the end of training. Furthermore, we used lateral radiographs to measure the tibial slope angle (TSA) and Insall-Salvati ratio (ISR) as indicators of patellar tendon shortening before surgery and after implant removal at 1 year after the operation [] (Fig. ). Measurement of knee ROM was performed using goniometry, and the landmarks used in the measurements were the greater trochanter of the femur, proximal head of the fibula, and lateral malleolus. Goniometry was used because it has been reported that goniometric measurements of ROM are more reliable than visual observation, with an accuracy of up to 1.0 degree []. The maximal IKEMS of the operated leg was assessed with the patient in a sitting position, with the hips and knees flexed at 90 degrees. A μTas F-1 handheld dynamometer (Anima Corp., Tokyo, Japan) was fixed to the chair, and two measurements were recorded. Each trial lasted 3–5 seconds, with 30 seconds of rest between trials. The higher score of two valid trials was recorded. All measurements were performed by a single trained physical therapist to eliminate interobserver variability. The EL, VAS, IKEMS, and ROM results are shown in Table . The EL improved from 3 degrees preoperatively to 0 degrees at the end of the sixth HAL-SJ training session, but it returned to 3 degrees at 1 and 3 months after the end of the training. When we compared results obtained before training against those obtained after each of the six training sessions, we observed that three sessions produced improved EL and three sessions produced improved or relatively constant VAS scores immediately after training. However, for the other three sessions, the patient reported increased pain immediately after training, with the greatest increase in pain reported immediately after the first HAL-SJ training session, when the VAS score was 1.7 times higher immediately after training than before training. The EL improved after training sessions 1 and 3, when the patient reported increased knee pain (expressed as the VAS score). However, the EL did not change after training sessions 2 and 4, when the patient reported less knee pain (improved VAS score immediately after training). The patient did not refuse to undergo training because of increased pain. The IKEMS value was the largest preoperatively (17.6 kgf) and decreased to its lowest value (30% of the preoperative strength) before the first HAL-SJ intervention at 8 days after the operation. The IKEMS remained relatively constant throughout HAL-SJ training but recovered to the preoperative value during follow-up (18.7 and 16.6 kgf at 1 and 3 months, respectively, after completion of HAL-SJ training). The active ROM also recovered to the preoperative value by the end of the sixth HAL-SJ training session. Thereafter, the extension ROM did not change, but the flexion ROM was maintained or improved. The JOA score decreased from 60 points preoperatively to 55 points at discharge, but it improved with time, reaching 65 and 85 points at 1 and 3 months, respectively, after the end of HAL-SJ training. Whereas the TSA was maintained at 13.1 degrees before and after the surgery, the ISR decreased from 1.13 preoperatively to 0.97 postoperatively. At 6 months after surgery, the passive ROM was 0–135 degrees, and the JOA score was 90 points. There were no complications throughout the preparation, surgery, or rehabilitation process.
What is the patient's Creatinine Clearance using the Cockroft-Gault Equation in terms of mL/min? You should use the patient's adjusted body weight in kg instead of the patient's actual body weight if the patient is overweight or obese based on their BMI. If the patient's BMI's normal, set their adjusted body weight to the minimum of the ideal body and actual weight. If the patient is underweight, please set their adjusted body weight to their actual body weight.
Creatinine Clearance (Cockcroft-Gault Equation): CrCl = ((140 - age) * adjusted weight * (gender_coefficient)) / (serum creatinine * 72), where the gender_coefficient is 1 if male, and 0.85 if female | |
6 | 2 | Creatinine Clearance (Cockcroft-Gault Equation) | lab test | decimal | pmc-8217860-1 | Extracted | This is a 61-year-old woman who presented with diabetic symptoms and was misclassified as having type 1 diabetes with negative autoimmune-related type 1 diabetes antibodies (Tyrosine Phosphatase antibodies and Glutamic acid Decarboxylase antibodies). She was referred to our center due to uncontrolled diabetes despite the high doses of insulin and the coexistence of severe insulin resistance and decreased body mass index (BMI: 19.4 kg/m2). Age of presentation was 29 years and for the following 30 years she was treated with multiple daily insulin injections with high insulin requirements (5 IU/kg/day) together with metformin 2 g/day for 30 years, but constantly displaying poor glycemic control. Dyslipidemia was observed at the age of 35 years with raised cholesterol levels and severe hypertriglyceridemia despite intense lipid lowering therapy which lately consisted of the combination of fenofibrate 145 mg, rosuvastatin 40 mg/day and omega-3 fatty acids/day together with restricted fat intake. Hypertension was observed at the age of 5 years, and lately treated with the combination of nifedipine 120 mg/day, eplerenone 25 mg/day and hydrochlorothiazide 25 mg/day.
She also had micro- and macrovascular complications of diabetes indicating constantly insufficient glycemic control. She presented peripheral diabetic neuropathy (distal symmetric polyneuropathy) and nephropathy (eGFR: 43 ml/min, albuminuria: 314 mg/24 h). She also suffered from severe cardiovascular disease including peripheral artery disease and hypertrophic cardiomyopathy. Peripheral artery disease presented as intermittent claudication and carotid stenosis, for which she had a right carotid endarterectomy at the age of 52 years old. She was managed with clopidogrel 75 mg/day.
She had menarche at the age of 11, followed by irregular menstruation and then premature menopause at the age of 38. She also reported polycystic ovarian syndrome and never conceived. She underwent hysterectomy due to fibroids at the age of 54. She was diagnosed with osteoporosis at the age of 58 and has since received alendronate 70 mg/week.
It has not been possible to conduct genetic family screening. Her mother and her maternal aunt displayed a lipodystrophy phenotype with fat loss of upper and lower extremities, presented diabetes from the ages of 25 and 28 respectively, and both showed early presentation of cardiovascular disease, presenting as ischemic stroke at the age of 45 years old and myocardial infarction at the same age, respectively. Her mother had reproductive problems and six miscarriages. Two out of four sisters and one brother developed hypertension and dyslipidemia at a young age.
A genetic analysis for lipodystrophy was performed and included the sequence and deletion/duplication analysis of the following genes: ADRA2A, AGPAT2, AKT2, BSCL2, CAV1, CAVIN1, CIDEC, FBN1, KCNJ6, LIPE, LMNA, LMNB2, PCYT1A, PIK3R1, PLIN1, POLD1, PPARG, PSMB8, and ZMPSTE24. The analysis revealed a novel heterozygous mutation in the PPARG gene (c470A>G, p. Glu157Gly, exon3) (The University of Chicago Genetic Services Laboratory). This particular amino acid change has not been described in other patients with PPARG-related disorders, but a different pathogenic sequence change affecting the same amino acid residue (p. Glu157Asp) has been described in a family with PPARG-related lipodystrophy (). In our case the substitution of the negative charged glutamic acid at position 157 by the hydrophobic glycine could possibly lead to the formation of a non-functional protein responsible for the lipodystrophy phenotype. According to missense interpretation by experimental report classifier (MITER) the described mutation is associated with 78.6% probability of causing FPLD3 and 6.5-fold increased risk for type 2 diabetes mellitus.
Examination revealed clinical signs of lipodystrophy of upper and lower limbs and gluteal area. Facial fat and abdominal prominence were also noted. She also had phlebectasia, hirsutism and cervical acanthosis nigricans. The patient mentioned that this phenotype was present from the age of 20 years old. Blood pressure was 175/84 mmHg.She was underweighted with a BMI: 19.40 kg/m2 (weight: 46 kg, height: 154 cm) ().
To assess the degree of regional fat loss in this case, we compared the total and proportional fat content in defined body regions using Dual-energy X-ray absorptiometry (DXA) with a group of healthy, lean postmenopausal women (). The case has a relatively short stature and as a consequence a total lean mass not far from the lower end the 95% confidence interval of the comparators. The total fat mass was drastically lower giving a first indication of a lipodystrophic state. The visceral fat mass was similar to the comparators whilst the proportional fat content in extremities was drastically reduced showing the classic features of peripheral fat loss in partial lipodystrophy ().
At the time of the first evaluation biochemical measurements revealed glycated hemoglobin (HbA1C) of 10%, a total cholesterol of 132 mg/dl of which high density lipoprotein (HDL-C) was 25 mg/dl. There was severe hypertriglyceridemia at 2.919 mg/dl. Further tests confirmed chronic kidney disease (blood urea nitrogen: 49.6 mg/dl, creatinine: 1.3 mg/dl, eGFR: 43 ml/min) and albuminuria (314 mg/24 h).
We performed glucagon stimulation test which revealed residual insulin secretion (fasting C-peptide: 2.09 ng/ml, 6 min after 1 mg of glucagon infusion C-peptide: 3.13 ng/ml). Plasma leptin concentration was close to zero (0.43 ng/ml).
Abdominal ultrasound confirmed hepatic steatosis and transient elastography (fibroscan) detected liver stiffness of 18 Kpa. Abdominal Magnetic Resonance Imaging (MRI) was unremarkable apart from hepatomegaly with a liver percentage fat fraction of 9.4%, and an enlarged spleen (). Cardiac MRI revealed left ventricular hypertrophy (maximal wall thickness 17 mm) and myocardial fibrosis in the basal interventricular septum (LGE SCORE 1/48, LGE mass 2%). Two-dimensional echocardiography revealed severe left ventricular hypertrophy, minimal mitral regurgitation, and ejection fraction of 60% ().
After noting her poor glycemic control, her antidiabetic treatment was intensified with empagliflozin 10 mg/daily and liraglutide 1.8 mg/daily, but this resulted only in a slight improvement in glycemic control after 3 months (HbA1c: 9.3%), despite additional strict dietetic management, but without any change in insulin management. We did not observe any change in triglyceride (TG) levels.
Metreleptin was then initiated at 5 mg once daily on top of the current lipid and diabetes management. Glycemic control and hypertriglyceridemia improved within two months of treatment evidenced by decrease of HbA1C from 10 to 8.7% and the reduction of TG from a baseline value of 2.919 to 242 mg/dl. At six months there was further reduction in HbA1C (7.9%) and in TG (198 mg/dl). This improvement was sustained one year after treatment with metreleptin in the same dose (HbA1C: 8%, TG: 185 mg/dl-standard serum determinations are listed in ), (). Insulin doses were reduced from more than 5 to 2.22 IU/kg/day. Blood pressure was also better controlled without any change in anti-hypertensive medication.
At six months of metreleptin treatment a reduced liver fat content was observed (MRI estimated liver percentage fat fraction was reduced from 9.4 to 6.8%). However, liver stiffness assessed by transient elastography remained stable. A repeated DXA scan showed unchanged total fat mass content and cardiac MRI revealed no change (). Reduction in appetite following metreleptin treatment was reported. Hunger scales for the assessment of appetite were not used. Metreleptin treatment was well tolerated with no other adverse effects. | What is the patient's Creatinine Clearance using the Cockroft-Gault Equation in terms of mL/min? You should use the patient's adjusted body weight in kg instead of the patient's actual body weight if the patient is overweight or obese based on their BMI. If the patient's BMI's normal, set their adjusted body weight to the minimum of the ideal body and actual weight. If the patient is underweight, please set their adjusted body weight to their actual body weight. | {'sex': 'Female', 'age': [61, 'years'], 'weight': [46.0, 'kg'], 'height': [154.0, 'cm'], 'creatinine': [1.3, 'mg/dL']} | 33.001 | 31.351 | 34.651 | The formula for computing Cockcroft-Gault is given by CrCl = ((140 - age) * adjusted weight * (gender_coefficient)) / (serum creatinine * 72), where the gender_coefficient is 1 if male, and 0.85 if female. The serum creatinine concentration is in mg/dL.
The patient's gender is female, which means that the gender coefficient is 0.85.
The patient is 61 years old.
The concentration of creatinine is 1.3 mg/dL.
The formula for computing the patient's BMI is (weight)/(height * height), where weight is the patient's weight in kg and height is the patient's height in m.
The patient's height is 154.0 cm, which is 154.0 cm * 1 m / 100 cm = 1.54 m. The patient's weight is 46.0 kg. The patient's bmi is therefore 46.0 kg / (1.54 m * 1.54 m) = 19.396 kg/m^2.The patient's BMI is 19.4, indicating they are normal weight.
Because the patient is normal, we take take minimum of the ideal body weight and the patient's body as the patient's adjusted weight for the Cockroft-Gault Equation. Hence, the adjusted body weight is the minimum of the two giving us an adjusted body weight of 46.0 kg.
Using the Cockcroft-Gault equation:
CrCl = ((140 - age) * adjusted weight * gender_coefficient) / (serum creatinine * 72).
Plugging the patient's values gives us ((140 - 61) * 46.0 * 0.85) / (1.3 * 72) = 33.001 mL/min. Hence, the patient's creatinine clearance is 33.001 mL/min. | This is a 61-year-old woman who presented with diabetic symptoms and was misclassified as having type 1 diabetes with negative autoimmune-related type 1 diabetes antibodies (Tyrosine Phosphatase antibodies and Glutamic acid Decarboxylase antibodies). She was referred to our center due to uncontrolled diabetes despite the high doses of insulin and the coexistence of severe insulin resistance and decreased body mass index (BMI: 19.4 kg/m2). Age of presentation was 29 years and for the following 30 years she was treated with multiple daily insulin injections with high insulin requirements (5 IU/kg/day) together with metformin 2 g/day for 30 years, but constantly displaying poor glycemic control. Dyslipidemia was observed at the age of 35 years with raised cholesterol levels and severe hypertriglyceridemia despite intense lipid lowering therapy which lately consisted of the combination of fenofibrate 145 mg, rosuvastatin 40 mg/day and omega-3 fatty acids/day together with restricted fat intake. Hypertension was observed at the age of 5 years, and lately treated with the combination of nifedipine 120 mg/day, eplerenone 25 mg/day and hydrochlorothiazide 25 mg/day.
She also had micro- and macrovascular complications of diabetes indicating constantly insufficient glycemic control. She presented peripheral diabetic neuropathy (distal symmetric polyneuropathy) and nephropathy (eGFR: 43 ml/min, albuminuria: 314 mg/24 h). She also suffered from severe cardiovascular disease including peripheral artery disease and hypertrophic cardiomyopathy. Peripheral artery disease presented as intermittent claudication and carotid stenosis, for which she had a right carotid endarterectomy at the age of 52 years old. She was managed with clopidogrel 75 mg/day.
She had menarche at the age of 11, followed by irregular menstruation and then premature menopause at the age of 38. She also reported polycystic ovarian syndrome and never conceived. She underwent hysterectomy due to fibroids at the age of 54. She was diagnosed with osteoporosis at the age of 58 and has since received alendronate 70 mg/week.
It has not been possible to conduct genetic family screening. Her mother and her maternal aunt displayed a lipodystrophy phenotype with fat loss of upper and lower extremities, presented diabetes from the ages of 25 and 28 respectively, and both showed early presentation of cardiovascular disease, presenting as ischemic stroke at the age of 45 years old and myocardial infarction at the same age, respectively. Her mother had reproductive problems and six miscarriages. Two out of four sisters and one brother developed hypertension and dyslipidemia at a young age.
A genetic analysis for lipodystrophy was performed and included the sequence and deletion/duplication analysis of the following genes: ADRA2A, AGPAT2, AKT2, BSCL2, CAV1, CAVIN1, CIDEC, FBN1, KCNJ6, LIPE, LMNA, LMNB2, PCYT1A, PIK3R1, PLIN1, POLD1, PPARG, PSMB8, and ZMPSTE24. The analysis revealed a novel heterozygous mutation in the PPARG gene (c470A>G, p. Glu157Gly, exon3) (The University of Chicago Genetic Services Laboratory). This particular amino acid change has not been described in other patients with PPARG-related disorders, but a different pathogenic sequence change affecting the same amino acid residue (p. Glu157Asp) has been described in a family with PPARG-related lipodystrophy (). In our case the substitution of the negative charged glutamic acid at position 157 by the hydrophobic glycine could possibly lead to the formation of a non-functional protein responsible for the lipodystrophy phenotype. According to missense interpretation by experimental report classifier (MITER) the described mutation is associated with 78.6% probability of causing FPLD3 and 6.5-fold increased risk for type 2 diabetes mellitus.
Examination revealed clinical signs of lipodystrophy of upper and lower limbs and gluteal area. Facial fat and abdominal prominence were also noted. She also had phlebectasia, hirsutism and cervical acanthosis nigricans. The patient mentioned that this phenotype was present from the age of 20 years old. Blood pressure was 175/84 mmHg.She was underweighted with a BMI: 19.40 kg/m2 (weight: 46 kg, height: 154 cm) ().
To assess the degree of regional fat loss in this case, we compared the total and proportional fat content in defined body regions using Dual-energy X-ray absorptiometry (DXA) with a group of healthy, lean postmenopausal women (). The case has a relatively short stature and as a consequence a total lean mass not far from the lower end the 95% confidence interval of the comparators. The total fat mass was drastically lower giving a first indication of a lipodystrophic state. The visceral fat mass was similar to the comparators whilst the proportional fat content in extremities was drastically reduced showing the classic features of peripheral fat loss in partial lipodystrophy ().
At the time of the first evaluation biochemical measurements revealed glycated hemoglobin (HbA1C) of 10%, a total cholesterol of 132 mg/dl of which high density lipoprotein (HDL-C) was 25 mg/dl. There was severe hypertriglyceridemia at 2.919 mg/dl. Further tests confirmed chronic kidney disease (blood urea nitrogen: 49.6 mg/dl, creatinine: 1.3 mg/dl, eGFR: 43 ml/min) and albuminuria (314 mg/24 h).
We performed glucagon stimulation test which revealed residual insulin secretion (fasting C-peptide: 2.09 ng/ml, 6 min after 1 mg of glucagon infusion C-peptide: 3.13 ng/ml). Plasma leptin concentration was close to zero (0.43 ng/ml).
Abdominal ultrasound confirmed hepatic steatosis and transient elastography (fibroscan) detected liver stiffness of 18 Kpa. Abdominal Magnetic Resonance Imaging (MRI) was unremarkable apart from hepatomegaly with a liver percentage fat fraction of 9.4%, and an enlarged spleen (). Cardiac MRI revealed left ventricular hypertrophy (maximal wall thickness 17 mm) and myocardial fibrosis in the basal interventricular septum (LGE SCORE 1/48, LGE mass 2%). Two-dimensional echocardiography revealed severe left ventricular hypertrophy, minimal mitral regurgitation, and ejection fraction of 60% ().
After noting her poor glycemic control, her antidiabetic treatment was intensified with empagliflozin 10 mg/daily and liraglutide 1.8 mg/daily, but this resulted only in a slight improvement in glycemic control after 3 months (HbA1c: 9.3%), despite additional strict dietetic management, but without any change in insulin management. We did not observe any change in triglyceride (TG) levels.
Metreleptin was then initiated at 5 mg once daily on top of the current lipid and diabetes management. Glycemic control and hypertriglyceridemia improved within two months of treatment evidenced by decrease of HbA1C from 10 to 8.7% and the reduction of TG from a baseline value of 2.919 to 242 mg/dl. At six months there was further reduction in HbA1C (7.9%) and in TG (198 mg/dl). This improvement was sustained one year after treatment with metreleptin in the same dose (HbA1C: 8%, TG: 185 mg/dl-standard serum determinations are listed in ), (). Insulin doses were reduced from more than 5 to 2.22 IU/kg/day. Blood pressure was also better controlled without any change in anti-hypertensive medication.
At six months of metreleptin treatment a reduced liver fat content was observed (MRI estimated liver percentage fat fraction was reduced from 9.4 to 6.8%). However, liver stiffness assessed by transient elastography remained stable. A repeated DXA scan showed unchanged total fat mass content and cardiac MRI revealed no change (). Reduction in appetite following metreleptin treatment was reported. Hunger scales for the assessment of appetite were not used. Metreleptin treatment was well tolerated with no other adverse effects.
What is the patient's Creatinine Clearance using the Cockroft-Gault Equation in terms of mL/min? You should use the patient's adjusted body weight in kg instead of the patient's actual body weight if the patient is overweight or obese based on their BMI. If the patient's BMI's normal, set their adjusted body weight to the minimum of the ideal body and actual weight. If the patient is underweight, please set their adjusted body weight to their actual body weight.
Creatinine Clearance (Cockcroft-Gault Equation): CrCl = ((140 - age) * adjusted weight * (gender_coefficient)) / (serum creatinine * 72), where the gender_coefficient is 1 if male, and 0.85 if female | |
7 | 2 | Creatinine Clearance (Cockcroft-Gault Equation) | lab test | decimal | pmc-6967248-1 | Extracted | A 53-year old man (height, 175 cm; weight, 87 kg) was scheduled to undergo subtotal stomach-preserving pancreatoduodenectomy with portal vein reconstruction for pancreatic cancer after receiving neoadjuvant chemotherapy with gemcitabine and nab-paclitaxel. Laparoscopic left nephrectomy for renal cell carcinoma was performed 1 year prior; therefore, harvesting the left internal jugular vein for portal vein reconstruction was planned because the left renal vein was too short. Preoperative serum creatinine level and potassium level were 1.39 mg/dL and 4.1 mEq/L, respectively.
General anesthesia was induced rapidly with propofol, rocuronium, fentanyl, and remifentanil and maintained with desflurane. The patient’s vital signs remained stable while resection of the distal stomach, gallbladder, distal common bile duct, and pancreatic head was performed. Bleeding from the first jejunal vein (J1V) occurred during adhesion detachment around the superior mesenteric vein (SMV), and clamping of the J1V was required to control the bleeding. Immediately after J1V clamping, bowel congestion progressed because the patient’s intestinal blood flow had been bypassed from the SMV to the inferior pancreaticoduodenal vein through J1V due to complete obstruction of the portal vein by the tumor. Therefore, a heparin-coated bypass tube (ANTHRON™ bypass tube, TORAY MEDICAL Co., Tokyo, Japan) was inserted from the SMV to the right great saphenous vein to relieve the bowel congestion. Several minutes after insertion of the ANTHRON™ bypass tube, blood potassium level rose from 4.7 mEq/L to 6.0 mEq/L, and pulseless ventricular tachycardia occurred. Chest compression was promptly performed by surgeons, and anesthesiologists attempted direct current defibrillation several times; epinephrine, magnesium sulphate, bicarbonate, lidocaine, and amiodarone were also administered. In addition to resuscitation, anesthesiologists inserted a blood-access catheter to the right internal jugular vein and started continuous renal replacement therapy to prevent elevation of blood potassium level. Spontaneous circulation was recovered after 30 min. The surgical team decided to discontinue the surgery, and the patient was transferred to the intensive care unit (ICU) after packing gauze into the abdomen and with the ANTHRON™ bypass tube left inserted. Total blood loss was 5620 mL, and total fluid balance was + 6115 mL. The operation time was 10 h 30 min.
Two days after the first operation, the patient was scheduled to undergo tumor resection and portal vein reconstruction with REIV. The surgical team abandoned using the left internal jugular vein for portal vein reconstruction because of concerns that brain congestion after harvesting the jugular vein could affect brain function recovery. Anesthesia was maintained with dexmedetomidine, fentanyl, rocuronium, and remifentanil. Continuous hemodiafiltration had been performed in the ICU due to persistent anuria and continued during the operation to prevent hyperkalemia. Both legs were compressed with a pneumatic compression device throughout the operation to prevent deep venous thrombosis formation. A section of the REIV 5 cm in length was harvested intraperitoneally with a surgical stapler, and the REIV distal end was closed with a 4-0 polypropylene running suture. The inferior epigastric vein, pubic branch of the obturator vein, and the deep circumflex iliac vein were preserved. A surgical nurse noticed swelling of the patient’s right leg 2 h after harvesting; the surgical team ensured careful observation throughout the surgery because a transient change by congestion of the right leg was suspected. Blood potassium level was slightly elevated after REIV resection, but ventricular arrhythmia was absent. Surgery was completed as scheduled (operation time, 7 h 3 min), and the patient was transferred to the ICU again. Total blood loss and total fluid balance were 2485 mL and + 2587 mL, respectively.
On ICU admission, distention and fullness of the right leg worsened. An orthopedist diagnosed the patient with acute compartment syndrome, and right leg elevation to lower the intracompartmental pressure was initiated. Blood potassium level was rapidly elevated immediately after leg elevation (Fig. ), which caused sustained ventricular tachycardia despite efforts to lower blood potassium level such as the administration of bicarbonate, glucose-insulin, and continuous hemodialysis with potassium-free dialysate. Chest compressions were initiated immediately. Ventricular tachycardia was prolonged; therefore, veno-arterial extracorporeal membrane oxygenation (V-A ECMO) was induced, and spontaneous circulation was recovered after resolution of hyperkalemia (Fig. , Table ). Emergent fasciotomy was performed by orthopedists 1 h after induction of V-A ECMO because the intracompartmental tissue pressure of the anterior compartment was 70 mmHg.
V-A ECMO was withdrawn 2 days later, and the patient was extubated 10 days after portal vein reconstruction. He had no apparent neural deficits; however, paralysis and paresthesia of the right leg persisted after discharge from the ICU 17 days post-operatively. | What is the patient's Creatinine Clearance using the Cockroft-Gault Equation in terms of mL/min? You should use the patient's adjusted body weight in kg instead of the patient's actual body weight if the patient is overweight or obese based on their BMI. If the patient's BMI's normal, set their adjusted body weight to the minimum of the ideal body and actual weight. If the patient is underweight, please set their adjusted body weight to their actual body weight. | {'sex': 'Male', 'weight': [87.0, 'kg'], 'height': [175.0, 'cm'], 'creatinine': [1.39, 'mg/dL'], 'age': [53, 'years']} | 67.005 | 63.655 | 70.355 | The formula for computing Cockcroft-Gault is given by CrCl = ((140 - age) * adjusted weight * (gender_coefficient)) / (serum creatinine * 72), where the gender_coefficient is 1 if male, and 0.85 if female. The serum creatinine concentration is in mg/dL.
The patient's gender is male, which means that the gender coefficient is 1.
The patient is 53 years old.
The concentration of creatinine is 1.39 mg/dL.
The formula for computing the patient's BMI is (weight)/(height * height), where weight is the patient's weight in kg and height is the patient's height in m.
The patient's height is 175.0 cm, which is 175.0 cm * 1 m / 100 cm = 1.75 m. The patient's weight is 87.0 kg. The patient's bmi is therefore 87.0 kg / (1.75 m * 1.75 m) = 28.408 kg/m^2.The patient's BMI is 28.4, indicating they are overweight/obese.
Because the patient is overweight/obese, we use the adjusted body weight formula to get the adjusted weight used for Cockroft-Gault Equation. Shown below is the computation for IBW (ideal body weight).
The patient's gender is Male.
The patient's height is 175.0 cm, which is 175.0 cm * 0.393701 in/cm = 68.898 in.
For males, the ideal body weight (IBW) is calculated as follows:
IBW = 50 kg + 2.3 kg * (height (in inches) - 60)
Plugging in the values gives us 50 kg + 2.3 kg * (68.898 (in inches) - 60) = 70.465 kg.
Hence, the patient's IBW is 70.465 kg.Shown below is the computation for ABW (adjusted body weight).
To compute the ABW value, apply the following formula: ABW = IBW + 0.4 * (weight (in kg) - IBW (in kg)). ABW = 70.465 kg + 0.4 * (87.0 kg - 70.465 kg) = 77.079 kg. The patient's adjusted body weight is 77.079 kg.
Using the Cockcroft-Gault equation:
CrCl = ((140 - age) * adjusted weight * gender_coefficient) / (serum creatinine * 72).
Plugging the patient's values gives us ((140 - 53) * 77.079 * 1) / (1.39 * 72) = 67.005 mL/min. Hence, the patient's creatinine clearance is 67.005 mL/min. | A 53-year old man (height, 175 cm; weight, 87 kg) was scheduled to undergo subtotal stomach-preserving pancreatoduodenectomy with portal vein reconstruction for pancreatic cancer after receiving neoadjuvant chemotherapy with gemcitabine and nab-paclitaxel. Laparoscopic left nephrectomy for renal cell carcinoma was performed 1 year prior; therefore, harvesting the left internal jugular vein for portal vein reconstruction was planned because the left renal vein was too short. Preoperative serum creatinine level and potassium level were 1.39 mg/dL and 4.1 mEq/L, respectively.
General anesthesia was induced rapidly with propofol, rocuronium, fentanyl, and remifentanil and maintained with desflurane. The patient’s vital signs remained stable while resection of the distal stomach, gallbladder, distal common bile duct, and pancreatic head was performed. Bleeding from the first jejunal vein (J1V) occurred during adhesion detachment around the superior mesenteric vein (SMV), and clamping of the J1V was required to control the bleeding. Immediately after J1V clamping, bowel congestion progressed because the patient’s intestinal blood flow had been bypassed from the SMV to the inferior pancreaticoduodenal vein through J1V due to complete obstruction of the portal vein by the tumor. Therefore, a heparin-coated bypass tube (ANTHRON™ bypass tube, TORAY MEDICAL Co., Tokyo, Japan) was inserted from the SMV to the right great saphenous vein to relieve the bowel congestion. Several minutes after insertion of the ANTHRON™ bypass tube, blood potassium level rose from 4.7 mEq/L to 6.0 mEq/L, and pulseless ventricular tachycardia occurred. Chest compression was promptly performed by surgeons, and anesthesiologists attempted direct current defibrillation several times; epinephrine, magnesium sulphate, bicarbonate, lidocaine, and amiodarone were also administered. In addition to resuscitation, anesthesiologists inserted a blood-access catheter to the right internal jugular vein and started continuous renal replacement therapy to prevent elevation of blood potassium level. Spontaneous circulation was recovered after 30 min. The surgical team decided to discontinue the surgery, and the patient was transferred to the intensive care unit (ICU) after packing gauze into the abdomen and with the ANTHRON™ bypass tube left inserted. Total blood loss was 5620 mL, and total fluid balance was + 6115 mL. The operation time was 10 h 30 min.
Two days after the first operation, the patient was scheduled to undergo tumor resection and portal vein reconstruction with REIV. The surgical team abandoned using the left internal jugular vein for portal vein reconstruction because of concerns that brain congestion after harvesting the jugular vein could affect brain function recovery. Anesthesia was maintained with dexmedetomidine, fentanyl, rocuronium, and remifentanil. Continuous hemodiafiltration had been performed in the ICU due to persistent anuria and continued during the operation to prevent hyperkalemia. Both legs were compressed with a pneumatic compression device throughout the operation to prevent deep venous thrombosis formation. A section of the REIV 5 cm in length was harvested intraperitoneally with a surgical stapler, and the REIV distal end was closed with a 4-0 polypropylene running suture. The inferior epigastric vein, pubic branch of the obturator vein, and the deep circumflex iliac vein were preserved. A surgical nurse noticed swelling of the patient’s right leg 2 h after harvesting; the surgical team ensured careful observation throughout the surgery because a transient change by congestion of the right leg was suspected. Blood potassium level was slightly elevated after REIV resection, but ventricular arrhythmia was absent. Surgery was completed as scheduled (operation time, 7 h 3 min), and the patient was transferred to the ICU again. Total blood loss and total fluid balance were 2485 mL and + 2587 mL, respectively.
On ICU admission, distention and fullness of the right leg worsened. An orthopedist diagnosed the patient with acute compartment syndrome, and right leg elevation to lower the intracompartmental pressure was initiated. Blood potassium level was rapidly elevated immediately after leg elevation (Fig. ), which caused sustained ventricular tachycardia despite efforts to lower blood potassium level such as the administration of bicarbonate, glucose-insulin, and continuous hemodialysis with potassium-free dialysate. Chest compressions were initiated immediately. Ventricular tachycardia was prolonged; therefore, veno-arterial extracorporeal membrane oxygenation (V-A ECMO) was induced, and spontaneous circulation was recovered after resolution of hyperkalemia (Fig. , Table ). Emergent fasciotomy was performed by orthopedists 1 h after induction of V-A ECMO because the intracompartmental tissue pressure of the anterior compartment was 70 mmHg.
V-A ECMO was withdrawn 2 days later, and the patient was extubated 10 days after portal vein reconstruction. He had no apparent neural deficits; however, paralysis and paresthesia of the right leg persisted after discharge from the ICU 17 days post-operatively.
What is the patient's Creatinine Clearance using the Cockroft-Gault Equation in terms of mL/min? You should use the patient's adjusted body weight in kg instead of the patient's actual body weight if the patient is overweight or obese based on their BMI. If the patient's BMI's normal, set their adjusted body weight to the minimum of the ideal body and actual weight. If the patient is underweight, please set their adjusted body weight to their actual body weight.
Creatinine Clearance (Cockcroft-Gault Equation): CrCl = ((140 - age) * adjusted weight * (gender_coefficient)) / (serum creatinine * 72), where the gender_coefficient is 1 if male, and 0.85 if female | |
8 | 2 | Creatinine Clearance (Cockcroft-Gault Equation) | lab test | decimal | pmc-6197009-1 | Extracted | A 51-year-old lady presented to our emergency department because of generalized body ache and marked weakness in both lower extremities for two days duration. She had no history of vomiting, diarrhea, frequent urination, recent use of laxatives or diuretics, current or previous use of lithium, licorice ingestion, or activities leading to profuse sweating. Past medical history was significant for type 2 diabetes mellitus, hypertension, seizure disorder and schizoaffective disorder. She also had a long-term history of alcoholism, consuming two to three pints of vodka every day for about 20 years. Her last drink of alcohol was about 48 hours prior to presentation. On examination, her weight was 79 kg, height 65 inches, body mass index 29.3 kg/m2. Vital signs were stable, temp 98.6°F, heart rate 68 bpm, respiratory rate 18, blood pressure 113/71 mmHg and oxygen saturation 98% on room air. She was alert and oriented, there was no thyromegaly or lymphadenopathy. Cardiac examination revealed a regular sinus rhythm with no murmurs. There were no deformities or edema of the extremities and distal pulses were present. There was no cushingoid facies, buffalo hump or abdominal striae noted. Neurological examination revealed bilateral lower limb weakness of 4/5, with intact sensory system and reflexes. Cranial nerve examination was unremarkable.
Biochemical analysis of the serum showed severe electrolyte disturbances, a potassium level of 2.3 mmol/L (reference 3.6−5.1 mmol/L), magnesium level of 0.9 mg/dL (reference 1.8−3.0 mg/dL), phosphorus level of 2.0 mg/dL (reference 2.4−4.6 mg/dL), corrected calcium level of 7.8 mg/dL (reference 8.9−10.3 mg/dL). Renal function was mildly deranged with Creatinine of 1.35 mg/dL (reference 0.4−1.3 mg/dL) and BUN of 12 mg/dL (reference 8−20mg/dL). The results of hepatic enzymes, AST 113 IU/l (reference 15−41 IU/l), ALT 42 IU/l (reference 17−63 IU/l) was suggestive of alcohol induced hepatic damage. Electrocardiogram (ECG) () showed no arrhythmias, but changes characteristic of hypokalemia with increased amplitude of the U-wave and marked corrected QT segment prolongation (QTc 551 ms). Patient was admitted to intensive care unit for severe hypokalemia management and cardiac monitoring. Aggressive supplementation of electrolytes was initiated (), however despite supplementation with enteral and parenteral potassium as well as magnesium and phosphate, potassium level failed to increase () and subsequently she had a sinus bradycardia followed by asystole. Cardiopulmonary resuscitation was initiated when asystole was noted, return of spontaneous circulation was obtained after 8 minutes of resuscitation. Patient was mechanically ventilated for two days and her own efficient respiration was reestablished, then she was successfully extubated. During the following days, the patient was conscious, alert and oriented to time, place and person. Further laboratory testing revealed thyroid- stimulating hormone level was 1.100 mIU/L (reference 0.45−4.50 mIU/L). Active renin level was 0.653ng/ml/hr (reference 0.167−5.38 ng/ml/hr), aldosterone levels was <0.01 ng/dL (reference 0.00− 30 ng/dL). Creatine kinase (CK) level was 6922 U/L (reference 38–297 IU/L), indicating rhabdomyolysis. The arterial blood gas analysis revealed pH of 7.430, partial pressure of carbon dioxide was 29 mmHg; partial pressure of oxygen was 74 mmHg; HCO3 was 25 mmol/L and base excess of -4.7 mmol/L. Urinalysis showed dilute urine of 1.010 g/mL specific gravity (reference 1.005 to 1.030), Urine pH of 6.5, and no proteinuria. Urine electrolytes were measured on spot urine analysis and twenty-four-hour urine collection, result depicted in . Serial electrocardiogram monitoring showed resolution of ECG changes (). Follow up laboratory tests revealed normalization of electrolytes level (). Post cardiac arrest serial ECGs didn’t reveal any ischemic changes, cardiac enzymes were not elevated and echocardiogram revealed normal left ventricular systolic function, Ejection Fraction of 60–65%. Cardiac arrest was presumed to be secondary to severe hypokalemia and there was no necessity for further cardiac evaluation. She was then discharged from the hospital with recommendations for abstinence from alcohol. Follow up outpatient appointment with primary care physician was provided. | What is the patient's Creatinine Clearance using the Cockroft-Gault Equation in terms of mL/min? You should use the patient's adjusted body weight in kg instead of the patient's actual body weight if the patient is overweight or obese based on their BMI. If the patient's BMI's normal, set their adjusted body weight to the minimum of the ideal body and actual weight. If the patient is underweight, please set their adjusted body weight to their actual body weight. | {'sex': 'Female', 'weight': [79.0, 'kg'], 'height': [65.0, 'in'], 'creatinine': [1.35, 'mg/dL'], 'age': [51, 'years']} | 51.212 | 48.651 | 53.773 | The formula for computing Cockcroft-Gault is given by CrCl = ((140 - age) * adjusted weight * (gender_coefficient)) / (serum creatinine * 72), where the gender_coefficient is 1 if male, and 0.85 if female. The serum creatinine concentration is in mg/dL.
The patient's gender is female, which means that the gender coefficient is 0.85.
The patient is 51 years old.
The concentration of creatinine is 1.35 mg/dL.
The formula for computing the patient's BMI is (weight)/(height * height), where weight is the patient's weight in kg and height is the patient's height in m.
The patient's height is 65.0 in, which is 65.0 in * 0.0254 m / in = 1.651 m. The patient's weight is 79.0 kg. The patient's bmi is therefore 79.0 kg / (1.651 m * 1.651 m) = 28.982 kg/m^2.The patient's BMI is 29.0, indicating they are overweight/obese.
Because the patient is overweight/obese, we use the adjusted body weight formula to get the adjusted weight used for Cockroft-Gault Equation. Shown below is the computation for IBW (ideal body weight).
The patient's gender is Female.
The patient's height is 65.0 in.
For females, the ideal body weight (IBW) is calculated as follows:
IBW = 45.5 kg + 2.3 kg * (height (in inches) - 60)
Plugging in the values gives us 45.5 kg + 2.3 kg * (65.0 (in inches) - 60) = 57.0 kg.
Hence, the patient's IBW is 57.0 kg.Shown below is the computation for ABW (adjusted body weight).
To compute the ABW value, apply the following formula: ABW = IBW + 0.4 * (weight (in kg) - IBW (in kg)). ABW = 57.0 kg + 0.4 * (79.0 kg - 57.0 kg) = 65.8 kg. The patient's adjusted body weight is 65.8 kg.
Using the Cockcroft-Gault equation:
CrCl = ((140 - age) * adjusted weight * gender_coefficient) / (serum creatinine * 72).
Plugging the patient's values gives us ((140 - 51) * 65.8 * 0.85) / (1.35 * 72) = 51.212 mL/min. Hence, the patient's creatinine clearance is 51.212 mL/min. | A 51-year-old lady presented to our emergency department because of generalized body ache and marked weakness in both lower extremities for two days duration. She had no history of vomiting, diarrhea, frequent urination, recent use of laxatives or diuretics, current or previous use of lithium, licorice ingestion, or activities leading to profuse sweating. Past medical history was significant for type 2 diabetes mellitus, hypertension, seizure disorder and schizoaffective disorder. She also had a long-term history of alcoholism, consuming two to three pints of vodka every day for about 20 years. Her last drink of alcohol was about 48 hours prior to presentation. On examination, her weight was 79 kg, height 65 inches, body mass index 29.3 kg/m2. Vital signs were stable, temp 98.6°F, heart rate 68 bpm, respiratory rate 18, blood pressure 113/71 mmHg and oxygen saturation 98% on room air. She was alert and oriented, there was no thyromegaly or lymphadenopathy. Cardiac examination revealed a regular sinus rhythm with no murmurs. There were no deformities or edema of the extremities and distal pulses were present. There was no cushingoid facies, buffalo hump or abdominal striae noted. Neurological examination revealed bilateral lower limb weakness of 4/5, with intact sensory system and reflexes. Cranial nerve examination was unremarkable.
Biochemical analysis of the serum showed severe electrolyte disturbances, a potassium level of 2.3 mmol/L (reference 3.6−5.1 mmol/L), magnesium level of 0.9 mg/dL (reference 1.8−3.0 mg/dL), phosphorus level of 2.0 mg/dL (reference 2.4−4.6 mg/dL), corrected calcium level of 7.8 mg/dL (reference 8.9−10.3 mg/dL). Renal function was mildly deranged with Creatinine of 1.35 mg/dL (reference 0.4−1.3 mg/dL) and BUN of 12 mg/dL (reference 8−20mg/dL). The results of hepatic enzymes, AST 113 IU/l (reference 15−41 IU/l), ALT 42 IU/l (reference 17−63 IU/l) was suggestive of alcohol induced hepatic damage. Electrocardiogram (ECG) () showed no arrhythmias, but changes characteristic of hypokalemia with increased amplitude of the U-wave and marked corrected QT segment prolongation (QTc 551 ms). Patient was admitted to intensive care unit for severe hypokalemia management and cardiac monitoring. Aggressive supplementation of electrolytes was initiated (), however despite supplementation with enteral and parenteral potassium as well as magnesium and phosphate, potassium level failed to increase () and subsequently she had a sinus bradycardia followed by asystole. Cardiopulmonary resuscitation was initiated when asystole was noted, return of spontaneous circulation was obtained after 8 minutes of resuscitation. Patient was mechanically ventilated for two days and her own efficient respiration was reestablished, then she was successfully extubated. During the following days, the patient was conscious, alert and oriented to time, place and person. Further laboratory testing revealed thyroid- stimulating hormone level was 1.100 mIU/L (reference 0.45−4.50 mIU/L). Active renin level was 0.653ng/ml/hr (reference 0.167−5.38 ng/ml/hr), aldosterone levels was <0.01 ng/dL (reference 0.00− 30 ng/dL). Creatine kinase (CK) level was 6922 U/L (reference 38–297 IU/L), indicating rhabdomyolysis. The arterial blood gas analysis revealed pH of 7.430, partial pressure of carbon dioxide was 29 mmHg; partial pressure of oxygen was 74 mmHg; HCO3 was 25 mmol/L and base excess of -4.7 mmol/L. Urinalysis showed dilute urine of 1.010 g/mL specific gravity (reference 1.005 to 1.030), Urine pH of 6.5, and no proteinuria. Urine electrolytes were measured on spot urine analysis and twenty-four-hour urine collection, result depicted in . Serial electrocardiogram monitoring showed resolution of ECG changes (). Follow up laboratory tests revealed normalization of electrolytes level (). Post cardiac arrest serial ECGs didn’t reveal any ischemic changes, cardiac enzymes were not elevated and echocardiogram revealed normal left ventricular systolic function, Ejection Fraction of 60–65%. Cardiac arrest was presumed to be secondary to severe hypokalemia and there was no necessity for further cardiac evaluation. She was then discharged from the hospital with recommendations for abstinence from alcohol. Follow up outpatient appointment with primary care physician was provided.
What is the patient's Creatinine Clearance using the Cockroft-Gault Equation in terms of mL/min? You should use the patient's adjusted body weight in kg instead of the patient's actual body weight if the patient is overweight or obese based on their BMI. If the patient's BMI's normal, set their adjusted body weight to the minimum of the ideal body and actual weight. If the patient is underweight, please set their adjusted body weight to their actual body weight.
Creatinine Clearance (Cockcroft-Gault Equation): CrCl = ((140 - age) * adjusted weight * (gender_coefficient)) / (serum creatinine * 72), where the gender_coefficient is 1 if male, and 0.85 if female | |
9 | 2 | Creatinine Clearance (Cockcroft-Gault Equation) | lab test | decimal | pmc-2547098-1 | Extracted | A 43-years-old Caucasian male (height 198 cm, weight 115 kg, tobacco smoker – 1 packet of cigarettes/day) was admitted to the intensive care unit (ICU) of a university hospital from a municipal hospital because of multiorgan dysfunction syndrome associated with infection and necrosis of the skin, subcutaneous tissue, and fascia of the left lower leg. The signs and symptoms of the disease – edema and pain affecting the left leg-began 7 days before admission. The patient's medical history was significant for hepatitis C (HCV), treated with ribavarin and interferon, and diabetes mellitus treated with insulin. On the day of admission the HCV-RNA test was negative. A mosquito bite was the probable triggering event.
On admission to the ICU the patient was confused, with a Glasgow Coma Scale (GCS) of 9. He was afebrile, had tachycardia, with a heart rate of 120 beats per minute, hypotension, with a blood pressure of 90/50 mmHg, and relative respiratory insufficiency (oxygen saturation of 88% – 90%). He had moderately-dilated pupils with a delayed light reflex. We noted crepitus over the bilateral lung fields, a tender abdomen with absent bowel sounds, and oliguria. There were numerous hemorrhagic extravasations on the skin. Examination of the left leg revealed diffuse edema of the skin, with marked erythema and necrosis; margins of infection were sharply demarcated, spreading onto the buttock and perineum on the left side (Figure ). Laboratory tests showed a metabolic acidosis, with the following values: base excess -15 mmol/l, lactate level 7.3 mmol/l, PaO2 64 mmHg, platelet count 29,000/mm3, International Normalized Ratio (INR) 2.24, serum creatinine 691.6 μmol/l, bilirubin 62.6 μmol/l, and C-reactive Protein (CRP) 224.6 μg/dl.
The Acute Physiology and Chronic Health Evaluation (APACHE) II score on the day of admission was 31 points and the Sequential Organ Failure Assessment (SOFA) score was 18 points. The patient required fluid resuscitation, endotracheal intubation, mechanical ventilation in BiPAP (bilevel positive airway pressure) mode, continuous intravenous infusion of catecholamines (epinephrine, norepinephrine) and low doses of steroids to restore blood pressure. After obtaining cultures from the affected tissue, blood and bronchoalveolar lavage (BAL) in appropriate media, empirical, broad-spectrum antibiotics were immediately administered (meropenem 3 g/day in a 3-h infusion, vancomycin 3 g/day in continuous infusion, metronidazole 1.5/day in 3 divided doses). Because of progressive organ dysfunction, therapy was started with activated protein C, in doses of 24 μg/kg/h; continuous veno-venous hemofiltration (CVVH) was also started. After several hours, the patient developed atrial fibrillation with a ventricular rate of 140 beats per minute and his blood pressure decreased to 80/50 mmHg. Electrical cardioversion was performed three times, followed by continuous infusion of cordarone (12 mg/kg/day). During this time, intensive fluid resuscitation was administered. During the first day, the patient received 12,800 ml of fluid (colloids and crystalloids). His unstable condition did not allow for early surgical management.
The cultures from the affected areas of skin contained Streptococcus pyogenes and Staphylococcus sciuri. Based on sensitivity results, vancomycin and metronidazole were discontinued, and penicillin G was started at a dose of 60 million units a day (intravenous) in 6 divided doses. Because the patient's poor condition persisted and the microbes were sensitive to clindamycin, it was added at 2.7 g/day in 3 divided doses. In spite of the lack of information about G-pathogens, meropenem was continued. The patient also received 40 g of commercially available gamma-globulin (intravenous), 8 units of packed red blood cells, 6 units of fresh frozen plasma, and 8 units of platelets. After several days his condition improved, with urine output of 100–150 ml/h and resolution of his metabolic acidosis. On the sixth day, the patient's hemodynamic parameters deteriorated again, with tachycardia to 160 beats per minute and a decrease in blood pressure to 85/60 mmHg. CVVH was administered again for detoxification. On the seventh day, the necrotic tissue was surgically excised (Figures , ). We also noted a progressive decline in the white blood cell count to 2,200/mm3, and administered granulocyte colony stimulating factor.
Cultures of the BAL showed 104 colony-forming units/ml of methycillin resistant Staphylococcus aureus (MRSA). (The patient had been a carrier of methycillin susceptible Staphylococcus aureus [MSSA] isolated from his nose vestibule on admission.) Because MRSA also was present in blood cultures and the patient's condition remained poor, linezolid 1.2 g a day in 2 divided doses was initiated based on additional results of susceptibility tests. After 10 days of intensive treatment, the patient was hemodynamically stable, and we discontinued mechanical ventilation. 25 days after admission the patient was discharged to the trauma surgery ward for plastic reconstruction of his wounds. | What is the patient's Creatinine Clearance using the Cockroft-Gault Equation in terms of mL/min? You should use the patient's adjusted body weight in kg instead of the patient's actual body weight if the patient is overweight or obese based on their BMI. If the patient's BMI's normal, set their adjusted body weight to the minimum of the ideal body and actual weight. If the patient is underweight, please set their adjusted body weight to their actual body weight. | {'sex': 'Male', 'age': [43, 'years'], 'weight': [115.0, 'kg'], 'height': [198.0, 'cm'], 'creatinine': [691.6, 'µmol/L']} | 17.406 | 16.536 | 18.276 | The formula for computing Cockcroft-Gault is given by CrCl = ((140 - age) * adjusted weight * (gender_coefficient)) / (serum creatinine * 72), where the gender_coefficient is 1 if male, and 0.85 if female. The serum creatinine concentration is in mg/dL.
The patient's gender is male, which means that the gender coefficient is 1.
The patient is 43 years old.
The concentration of creatinine is 691.6 µmol/L. We need to convert the concentration to mg/dL. Let's first convert the mass of creatinine from µmol to mg. The mass of creatinine is 691.6 µmol. To convert 691.6 µmol of creatinine to mol, multiply by the conversion factor 1e-06, giving us 691.6 µmol creatinine * 1e-06 mol/µmol = 0.000692 mol creatinine. To convert from mol creatinine to grams, multiply by the molar mass 113.12 g/mol, which will give 0.000692 mol creatinine * 113.12 g/mol = 0.078 g creatinine. To convert 0.078 g of creatinine to mg, multiply by the conversion factor 1000.0, giving us 0.078 g creatinine * 1000.0 mg/g = 78.0 mg creatinine. The current volume unit is L and the target volume unit is dL. The conversion factor is 10.0 dL for every unit of L. Our next step will be to divide the mass by the volume conversion factor of 10.0 to get the final concentration in terms of mg/dL. This will result to 78.0 mg creatinine/10.0 dL = 7.8 mg creatinine/dL. The concentration value of 691.6 µmol creatinine/L converts to 7.8 mg creatinine/dL.
The formula for computing the patient's BMI is (weight)/(height * height), where weight is the patient's weight in kg and height is the patient's height in m.
The patient's height is 198.0 cm, which is 198.0 cm * 1 m / 100 cm = 1.98 m. The patient's weight is 115.0 kg. The patient's bmi is therefore 115.0 kg / (1.98 m * 1.98 m) = 29.334 kg/m^2.The patient's BMI is 29.3, indicating they are overweight/obese.
Because the patient is overweight/obese, we use the adjusted body weight formula to get the adjusted weight used for Cockroft-Gault Equation. Shown below is the computation for IBW (ideal body weight).
The patient's gender is Male.
The patient's height is 198.0 cm, which is 198.0 cm * 0.393701 in/cm = 77.953 in.
For males, the ideal body weight (IBW) is calculated as follows:
IBW = 50 kg + 2.3 kg * (height (in inches) - 60)
Plugging in the values gives us 50 kg + 2.3 kg * (77.953 (in inches) - 60) = 91.292 kg.
Hence, the patient's IBW is 91.292 kg.Shown below is the computation for ABW (adjusted body weight).
To compute the ABW value, apply the following formula: ABW = IBW + 0.4 * (weight (in kg) - IBW (in kg)). ABW = 91.292 kg + 0.4 * (115.0 kg - 91.292 kg) = 100.775 kg. The patient's adjusted body weight is 100.775 kg.
Using the Cockcroft-Gault equation:
CrCl = ((140 - age) * adjusted weight * gender_coefficient) / (serum creatinine * 72).
Plugging the patient's values gives us ((140 - 43) * 100.775 * 1) / (7.8 * 72) = 17.406 mL/min. Hence, the patient's creatinine clearance is 17.406 mL/min. | A 43-years-old Caucasian male (height 198 cm, weight 115 kg, tobacco smoker – 1 packet of cigarettes/day) was admitted to the intensive care unit (ICU) of a university hospital from a municipal hospital because of multiorgan dysfunction syndrome associated with infection and necrosis of the skin, subcutaneous tissue, and fascia of the left lower leg. The signs and symptoms of the disease – edema and pain affecting the left leg-began 7 days before admission. The patient's medical history was significant for hepatitis C (HCV), treated with ribavarin and interferon, and diabetes mellitus treated with insulin. On the day of admission the HCV-RNA test was negative. A mosquito bite was the probable triggering event.
On admission to the ICU the patient was confused, with a Glasgow Coma Scale (GCS) of 9. He was afebrile, had tachycardia, with a heart rate of 120 beats per minute, hypotension, with a blood pressure of 90/50 mmHg, and relative respiratory insufficiency (oxygen saturation of 88% – 90%). He had moderately-dilated pupils with a delayed light reflex. We noted crepitus over the bilateral lung fields, a tender abdomen with absent bowel sounds, and oliguria. There were numerous hemorrhagic extravasations on the skin. Examination of the left leg revealed diffuse edema of the skin, with marked erythema and necrosis; margins of infection were sharply demarcated, spreading onto the buttock and perineum on the left side (Figure ). Laboratory tests showed a metabolic acidosis, with the following values: base excess -15 mmol/l, lactate level 7.3 mmol/l, PaO2 64 mmHg, platelet count 29,000/mm3, International Normalized Ratio (INR) 2.24, serum creatinine 691.6 μmol/l, bilirubin 62.6 μmol/l, and C-reactive Protein (CRP) 224.6 μg/dl.
The Acute Physiology and Chronic Health Evaluation (APACHE) II score on the day of admission was 31 points and the Sequential Organ Failure Assessment (SOFA) score was 18 points. The patient required fluid resuscitation, endotracheal intubation, mechanical ventilation in BiPAP (bilevel positive airway pressure) mode, continuous intravenous infusion of catecholamines (epinephrine, norepinephrine) and low doses of steroids to restore blood pressure. After obtaining cultures from the affected tissue, blood and bronchoalveolar lavage (BAL) in appropriate media, empirical, broad-spectrum antibiotics were immediately administered (meropenem 3 g/day in a 3-h infusion, vancomycin 3 g/day in continuous infusion, metronidazole 1.5/day in 3 divided doses). Because of progressive organ dysfunction, therapy was started with activated protein C, in doses of 24 μg/kg/h; continuous veno-venous hemofiltration (CVVH) was also started. After several hours, the patient developed atrial fibrillation with a ventricular rate of 140 beats per minute and his blood pressure decreased to 80/50 mmHg. Electrical cardioversion was performed three times, followed by continuous infusion of cordarone (12 mg/kg/day). During this time, intensive fluid resuscitation was administered. During the first day, the patient received 12,800 ml of fluid (colloids and crystalloids). His unstable condition did not allow for early surgical management.
The cultures from the affected areas of skin contained Streptococcus pyogenes and Staphylococcus sciuri. Based on sensitivity results, vancomycin and metronidazole were discontinued, and penicillin G was started at a dose of 60 million units a day (intravenous) in 6 divided doses. Because the patient's poor condition persisted and the microbes were sensitive to clindamycin, it was added at 2.7 g/day in 3 divided doses. In spite of the lack of information about G-pathogens, meropenem was continued. The patient also received 40 g of commercially available gamma-globulin (intravenous), 8 units of packed red blood cells, 6 units of fresh frozen plasma, and 8 units of platelets. After several days his condition improved, with urine output of 100–150 ml/h and resolution of his metabolic acidosis. On the sixth day, the patient's hemodynamic parameters deteriorated again, with tachycardia to 160 beats per minute and a decrease in blood pressure to 85/60 mmHg. CVVH was administered again for detoxification. On the seventh day, the necrotic tissue was surgically excised (Figures , ). We also noted a progressive decline in the white blood cell count to 2,200/mm3, and administered granulocyte colony stimulating factor.
Cultures of the BAL showed 104 colony-forming units/ml of methycillin resistant Staphylococcus aureus (MRSA). (The patient had been a carrier of methycillin susceptible Staphylococcus aureus [MSSA] isolated from his nose vestibule on admission.) Because MRSA also was present in blood cultures and the patient's condition remained poor, linezolid 1.2 g a day in 2 divided doses was initiated based on additional results of susceptibility tests. After 10 days of intensive treatment, the patient was hemodynamically stable, and we discontinued mechanical ventilation. 25 days after admission the patient was discharged to the trauma surgery ward for plastic reconstruction of his wounds.
What is the patient's Creatinine Clearance using the Cockroft-Gault Equation in terms of mL/min? You should use the patient's adjusted body weight in kg instead of the patient's actual body weight if the patient is overweight or obese based on their BMI. If the patient's BMI's normal, set their adjusted body weight to the minimum of the ideal body and actual weight. If the patient is underweight, please set their adjusted body weight to their actual body weight.
Creatinine Clearance (Cockcroft-Gault Equation): CrCl = ((140 - age) * adjusted weight * (gender_coefficient)) / (serum creatinine * 72), where the gender_coefficient is 1 if male, and 0.85 if female | |
10 | 2 | Creatinine Clearance (Cockcroft-Gault Equation) | lab test | decimal | pmc-6408197-1 | Extracted | A 65-year-old female consulted our office for naturopathic primary-care support for a myriad of conditions, which included diabetes with weight gain, chronic fatigue, depression with emotional lability, frequent colds, and recurrent urinary tract infections. The latter was attributed to a medullary sponge kidney as was her history of kidney stones and hypertension. The patient also suffered with long-standing acid reflux and was prone to irritable bowel with diarrhea. She had also suffered with multiple abscesses in the past as well as poor generalized wound healing. A history of fibroadenomas was also noted. The patient recollected, “never being well”, even as a child. She described her diet as a child as “deficient” and consisted mostly of canned beans and bread, which she attributed to her poor socioeconomic status as a child.
Pharmacological management of her diabetic condition included the use of metformin/sitagliptin (1,000 mg/50 mg, taken twice per day) and gliclazide (30 mg), also taken twice per day.
Additional medications included ramipril (5 mg/day), ranitidine (150 mg, twice per day), low-dose aspirin (81 mg/ day), hydrochlorothiazide (25 mg/day), allopurinol (100 mg/ day), citalopram (40 mg/day), and mirabegron (50 mg/day).
Physical examination revealed a 1.69 m (66.5 inch), 88.5 kg (195.0 lb) female. Body mass index was calculated at 31.0 (Obese Class I) (32). Central waist measurement was 112 cm, while her hips measured 118 cm. Blood pressure was 114/64 mmHg, measured at the left brachial artery. Bioimpedance analysis revealed a lean body mass of 49.9 kg (111.0 lbs) and a fat mass of 38.0 kg (84.0 lbs).
Laboratory assessment prior to date of initial consult (June 2017) revealed a HBA1C of 7.8% and a random glucose of 6.5 mmol/L. Total cholesterol (TC) was 4.68 mmol/L, triglycerides (TG) were 2.63 mmol/L, high-density lipoproteins (HDL) was 1.04 mmol/L, low-density lipoproteins (LDL) was 2.44 mmol/L, and TC:HDL was 4.5. Alanine aminotransferase was 55 U/L, while creatinine was 79 μmol/L. | What is the patient's Creatinine Clearance using the Cockroft-Gault Equation in terms of mL/min? You should use the patient's adjusted body weight in kg instead of the patient's actual body weight if the patient is overweight or obese based on their BMI. If the patient's BMI's normal, set their adjusted body weight to the minimum of the ideal body and actual weight. If the patient is underweight, please set their adjusted body weight to their actual body weight. | {'sex': 'Female', 'age': [65, 'years'], 'weight': [88.5, 'kg'], 'height': [1.69, 'm'], 'creatinine': [79.0, 'µmol/L']} | 70.556 | 67.028 | 74.084 | The formula for computing Cockcroft-Gault is given by CrCl = ((140 - age) * adjusted weight * (gender_coefficient)) / (serum creatinine * 72), where the gender_coefficient is 1 if male, and 0.85 if female. The serum creatinine concentration is in mg/dL.
The patient's gender is female, which means that the gender coefficient is 0.85.
The patient is 65 years old.
The concentration of creatinine is 79.0 µmol/L. We need to convert the concentration to mg/dL. Let's first convert the mass of creatinine from µmol to mg. The mass of creatinine is 79.0 µmol. To convert 79.0 µmol of creatinine to mol, multiply by the conversion factor 1e-06, giving us 79.0 µmol creatinine * 1e-06 mol/µmol = 7.9e-05 mol creatinine. To convert from mol creatinine to grams, multiply by the molar mass 113.12 g/mol, which will give 7.9e-05 mol creatinine * 113.12 g/mol = 0.009 g creatinine. To convert 0.009 g of creatinine to mg, multiply by the conversion factor 1000.0, giving us 0.009 g creatinine * 1000.0 mg/g = 9.0 mg creatinine. The current volume unit is L and the target volume unit is dL. The conversion factor is 10.0 dL for every unit of L. Our next step will be to divide the mass by the volume conversion factor of 10.0 to get the final concentration in terms of mg/dL. This will result to 9.0 mg creatinine/10.0 dL = 0.9 mg creatinine/dL. The concentration value of 79.0 µmol creatinine/L converts to 0.9 mg creatinine/dL.
The formula for computing the patient's BMI is (weight)/(height * height), where weight is the patient's weight in kg and height is the patient's height in m.
The patient's height is 1.69 m. The patient's weight is 88.5 kg. The patient's bmi is therefore 88.5 kg / (1.69 m * 1.69 m) = 30.986 kg/m^2.The patient's BMI is 31.0, indicating they are overweight/obese.
Because the patient is overweight/obese, we use the adjusted body weight formula to get the adjusted weight used for Cockroft-Gault Equation. Shown below is the computation for IBW (ideal body weight).
The patient's gender is Female.
The patient's height is 1.69 m, which is 1.69 m * 39.3701 in/m = 66.535 in.
For females, the ideal body weight (IBW) is calculated as follows:
IBW = 45.5 kg + 2.3 kg * (height (in inches) - 60)
Plugging in the values gives us 45.5 kg + 2.3 kg * (66.535 (in inches) - 60) = 60.53 kg.
Hence, the patient's IBW is 60.53 kg.Shown below is the computation for ABW (adjusted body weight).
To compute the ABW value, apply the following formula: ABW = IBW + 0.4 * (weight (in kg) - IBW (in kg)). ABW = 60.53 kg + 0.4 * (88.5 kg - 60.53 kg) = 71.718 kg. The patient's adjusted body weight is 71.718 kg.
Using the Cockcroft-Gault equation:
CrCl = ((140 - age) * adjusted weight * gender_coefficient) / (serum creatinine * 72).
Plugging the patient's values gives us ((140 - 65) * 71.718 * 0.85) / (0.9 * 72) = 70.556 mL/min. Hence, the patient's creatinine clearance is 70.556 mL/min. | A 65-year-old female consulted our office for naturopathic primary-care support for a myriad of conditions, which included diabetes with weight gain, chronic fatigue, depression with emotional lability, frequent colds, and recurrent urinary tract infections. The latter was attributed to a medullary sponge kidney as was her history of kidney stones and hypertension. The patient also suffered with long-standing acid reflux and was prone to irritable bowel with diarrhea. She had also suffered with multiple abscesses in the past as well as poor generalized wound healing. A history of fibroadenomas was also noted. The patient recollected, “never being well”, even as a child. She described her diet as a child as “deficient” and consisted mostly of canned beans and bread, which she attributed to her poor socioeconomic status as a child.
Pharmacological management of her diabetic condition included the use of metformin/sitagliptin (1,000 mg/50 mg, taken twice per day) and gliclazide (30 mg), also taken twice per day.
Additional medications included ramipril (5 mg/day), ranitidine (150 mg, twice per day), low-dose aspirin (81 mg/ day), hydrochlorothiazide (25 mg/day), allopurinol (100 mg/ day), citalopram (40 mg/day), and mirabegron (50 mg/day).
Physical examination revealed a 1.69 m (66.5 inch), 88.5 kg (195.0 lb) female. Body mass index was calculated at 31.0 (Obese Class I) (32). Central waist measurement was 112 cm, while her hips measured 118 cm. Blood pressure was 114/64 mmHg, measured at the left brachial artery. Bioimpedance analysis revealed a lean body mass of 49.9 kg (111.0 lbs) and a fat mass of 38.0 kg (84.0 lbs).
Laboratory assessment prior to date of initial consult (June 2017) revealed a HBA1C of 7.8% and a random glucose of 6.5 mmol/L. Total cholesterol (TC) was 4.68 mmol/L, triglycerides (TG) were 2.63 mmol/L, high-density lipoproteins (HDL) was 1.04 mmol/L, low-density lipoproteins (LDL) was 2.44 mmol/L, and TC:HDL was 4.5. Alanine aminotransferase was 55 U/L, while creatinine was 79 μmol/L.
What is the patient's Creatinine Clearance using the Cockroft-Gault Equation in terms of mL/min? You should use the patient's adjusted body weight in kg instead of the patient's actual body weight if the patient is overweight or obese based on their BMI. If the patient's BMI's normal, set their adjusted body weight to the minimum of the ideal body and actual weight. If the patient is underweight, please set their adjusted body weight to their actual body weight.
Creatinine Clearance (Cockcroft-Gault Equation): CrCl = ((140 - age) * adjusted weight * (gender_coefficient)) / (serum creatinine * 72), where the gender_coefficient is 1 if male, and 0.85 if female | |
11 | 2 | Creatinine Clearance (Cockcroft-Gault Equation) | lab test | decimal | pmc-8705311-1 | Extracted | An 18-year-old adolescent female was evaluated at 15 weeks’ gestation for history of persistent emesis for four weeks, extreme fatigue and red colored urine for one day. There was no history of fever, diarrhea, abdominal pain, or urinary tract infection.
Past medical history was unremarkable for diabetes mellitus, rheumatoid arthritis, or other autoimmune diseases. She was not known to have hyperthyroidism in the past. Pregnancy had been uneventful except for persistent episodes of emesis for past one month. There was no prior history of mood symptoms or altered mental status. There was no history of heat intolerance, diarrhea, or weight loss. There was no recent history of usage of corticosteroid, loop or thiazide diuretic, strenuous exercise, vaginal bleeding, vaginal discharge of grape-like vesicles, seizures, alcohol intake, and carbohydrate load. Family history was notable only for type 2 diabetes in the father. There was no known family history of autoimmune diseases, thyroid disorders, hypokalemia, and periodic paralysis. There was no consanguinity.
Vital signs upon presentation showed blood pressure (BP) 142/87 mm Hg, pulse 120 beats per minute, oral temperature 38.9 °C (102.02 °F), respiratory rate 18 per minute, and oxygen saturation of 97%. Her height was 172.7 cm and weight was 109 kg (240 lb 4.8 oz). Physical examination was remarkable for an overweight female who was awake but slow to respond. There was no goiter and ophthalmopathy. There was mild scleral icterus. There was no tremor or pretibial edema.
Serum beta-human chorionic gonadotropin (hCG) level was 246,000 mIU/mL and sonogram confirmed the presence of a single viable intrauterine fetus of approximately 15 weeks gestation with expected uterine size. Renal function test showed sodium 127 mmol/L, potassium 2.5 mmol/L, bicarbonate 33 mmol/L, blood urea nitrogen (BUN) 123 mg/dL, serum creatinine 4.2 mg/dL (MDRD estimated glomerular filtration rate (eGFR) 17 mL/min/1.73 m2), calcium 9.5 mg/dL, phosphorus 2.7 mg/dL and magnesium of 1 mg/dL. Liver function test showed aspartate aminotransferase 140 IU/L, alanine aminotransferase 203 IU/L, total bilirubin 2.9 mg/dL, ammonia 55 µmol/L, and serum albumin 3.1 gm/dl. Renal function test two months prior to pregnancy showed normal serum creatinine of 0.8 mg/dL (MDRD eGFR 113 mL/min/1.73 m2) and normal electrolytes (serum sodium 138 mmol/L, potassium 3.9 mmol/L, bicarbonate 24 mmol/L, calcium 9.4 mg/dL, phosphorus 3.9 mg/dL, and magnesium was not available) Serum creatine kinase was normal at 121 U/L (normal 0–180 U/L). Urine sodium was <10 mmol/L, urine creatinine 84 mg/dL, urine potassium 28 mmol/L and urine osmolality was 344 mOsm/kg. Fractional excretion of sodium was 0.4%. Urinalysis showed 1+ proteinuria, no microscopic hematuria, 5 white cells per high power field, no ketonuria, pH 5, specific gravity of 1.015, and negative nitrites and leukocytes. Plasma renin activity was 14 ng/mL/h (normal 0.5–4 ng/mL/h, upright) and serum aldosterone was 13 ng/dL (normal 4–31 ng/dL, upright). Blood and urine cultures were negative. Other extensive investigations for infectious etiologies were also negative. Urine for Chlamydia and Neisseria was negative. SARS-CoV-2 DNA PCR from the nasopharyngeal swab was negative. Other labs were notable for undetectable thyroid stimulating hormone (TSH) level < 0.030 mIU/L (reference 0.4–5 mIU/L), total T3 238 ng/dL (reference 87–178 ng/dL), and free T4 > 6.99 ng/dL (reference 0.6–1.2 ng/dL). Computed tomography of the head showed no acute intracranial abnormalities.
Initial management included administration of intravenous fluids (IVF), propranolol, potassium iodide, propylthiouracil (PTU), and hydrocortisone. A presumptive diagnosis of hyperemesis gravidarum with thyroid storm and AKI secondary to persistent emesis was made. She met criteria for thyroid storm due to elevated serum free T4 and total T3 with undetected TSH, along with pyrexia, tachycardia, icterus, and altered mental status. Her clinical condition improved somewhat after receiving PTU, propranolol, and hydrocortisone as heart rate, blood pressure, and free T4 began to decrease. Her mental status improved and she became more alert and engaged in conversation. Given tachycardia and hypertension, she was started on propranolol 60 mg every 4 hours which was later converted to 160 mg daily.
Other thyroid studies showed thyroid peroxidase antibody 0.3 IU/mL (reference < 9 IU/mL), TSH receptor antibody (TRAb) < 0.90 (reference < 1.75 IU/L), and undetected thyroid stimulating immunoglobulin (TSI) of < 0.10 (reference ≤ 0.54 IU/L). Given negative TRAb, Graves’ disease was highly unlikely. Serum free T4 normalized in ten days, TSH in two weeks and total T3 in five days. Given pregnancy, further modalities including radioactive iodine uptake study were not pursued, given risk of fetal hypothyroidism, mental retardation, and increased risk of malignancy. Partial molar pregnancy was initially considered due to presentation of thyroid storm, however, the beta-hCG level was trending down and the patient did not show any signs of pre-eclampsia. Thyroid sonogram showed normal sized thyroid with homogenous thyroid texture and without increased vascularity, making Grave’s disease unlikely. Investigations for AKI included renal sonogram which showed right kidney measuring 12.8 cm in length and left kidney measuring 12.6 cm in length with bilateral normal cortical echogenicity without evidence of hydronephrosis or nephrocalcinosis. Hepatic sonogram showed gallbladder sludge. A chest X-ray was normal without pulmonary edema or cardiomegaly. Electrocardiogram showed normal Q-T interval. Echocardiogram was normal with ejection fraction of 65%. Cardiac enzymes were normal.
PTU was later changed to methimazole as she was no longer in the first trimester of pregnancy and as she demonstrated signs of liver insufficiency. Anti-emetics and IVF were discontinued after few days as the patient was able to tolerate well by mouth. Hydrocortisone was discontinued after two days. Subsequently, propranolol was discontinued along with methimazole, as the beta-hCG mediated hyperemesis was thought to be the likely etiology of thyroid symptoms. Her vital signs, including BPs, remained stable and her thyroid levels returned to normal without anti-thyroid drugs. Serum beta-hCG at discharge was 175,557 mIU/mL. Given decreasing level of hCG without other signs or symptoms of gestational trophoblastic disease, molar pregnancy was unlikely. She was discharged without any thyroid medications.
During the hospitalization, her serum potassium remained around 2.4–2.9 meq/L along with serum bicarbonate 30–38 meq/L despite resolution of emesis. Serum magnesium remained low, as well as with values ranging from 1–1.4 mg/dL. Twenty-four hour urine collection showed a urine calcium of 0.04 mg/kg/day. Random urine calcium to creatinine ratio was also low at 0.005. She required multiple intravenous potassium and magnesium supplements. Discharge serum potassium and magnesium was 3.5 meq/L and 1.2 mg/dL, respectively. She was discharged on magnesium oxide 400 mg daily and potassium chloride 10 meq twice daily. BUN and serum creatinine slowly improved with intravenous hydration. Kidney biopsy was not performed and renal replacement therapy was not required. Discharge BUN and serum creatinine was 15 mg/dL and 0.97 mg/dL (MDRD eGFR 90 mL/min/1.73 m2), respectively. Due to the persistent hypokalemia, alkalosis, hypomagnesemia and hypocalciuria despite resolution of emesis, a genetic testing by next generation sequence analysis was done which showed that the patient was homozygous in the SLCA123 (NM_001126108.2) gene for a known sequence variant designated c.2581C>T (p.Arg861Cys) (Prevention Genetics, Marshfield, WI, USA). No further in vitro functional studies were performed, hence the exact functional implication of this variant was unknown. However, to determine the pathogenicity of this variant, in silico tests were performed using SIFT, PolyPhen-2, FATHMM and MutationTaster. The resulting prediction utilizing these in silico tools was “Pathogenic”. At 37 weeks gestation, a healthy infant of 3.5 kilograms was born vaginally without any perinatal complications. The serum creatinine remained stable at 0.7 mg/dL after delivery (MDRD eGFR 132 mL/min/1.73 m2). | What is the patient's Creatinine Clearance using the Cockroft-Gault Equation in terms of mL/min? You should use the patient's adjusted body weight in kg instead of the patient's actual body weight if the patient is overweight or obese based on their BMI. If the patient's BMI's normal, set their adjusted body weight to the minimum of the ideal body and actual weight. If the patient is underweight, please set their adjusted body weight to their actual body weight. | {'sex': 'Female', 'age': [18, 'years'], 'weight': [109.0, 'kg'], 'height': [172.7, 'cm'], 'creatinine': [4.2, 'mg/dL']} | 28.095 | 26.69 | 29.5 | The formula for computing Cockcroft-Gault is given by CrCl = ((140 - age) * adjusted weight * (gender_coefficient)) / (serum creatinine * 72), where the gender_coefficient is 1 if male, and 0.85 if female. The serum creatinine concentration is in mg/dL.
The patient's gender is female, which means that the gender coefficient is 0.85.
The patient is 18 years old.
The concentration of creatinine is 4.2 mg/dL.
The formula for computing the patient's BMI is (weight)/(height * height), where weight is the patient's weight in kg and height is the patient's height in m.
The patient's height is 172.7 cm, which is 172.7 cm * 1 m / 100 cm = 1.727 m. The patient's weight is 109.0 kg. The patient's bmi is therefore 109.0 kg / (1.727 m * 1.727 m) = 36.546 kg/m^2.The patient's BMI is 36.5, indicating they are overweight/obese.
Because the patient is overweight/obese, we use the adjusted body weight formula to get the adjusted weight used for Cockroft-Gault Equation. Shown below is the computation for IBW (ideal body weight).
The patient's gender is Female.
The patient's height is 172.7 cm, which is 172.7 cm * 0.393701 in/cm = 67.992 in.
For females, the ideal body weight (IBW) is calculated as follows:
IBW = 45.5 kg + 2.3 kg * (height (in inches) - 60)
Plugging in the values gives us 45.5 kg + 2.3 kg * (67.992 (in inches) - 60) = 63.882 kg.
Hence, the patient's IBW is 63.882 kg.Shown below is the computation for ABW (adjusted body weight).
To compute the ABW value, apply the following formula: ABW = IBW + 0.4 * (weight (in kg) - IBW (in kg)). ABW = 63.882 kg + 0.4 * (109.0 kg - 63.882 kg) = 81.929 kg. The patient's adjusted body weight is 81.929 kg.
Using the Cockcroft-Gault equation:
CrCl = ((140 - age) * adjusted weight * gender_coefficient) / (serum creatinine * 72).
Plugging the patient's values gives us ((140 - 18) * 81.929 * 0.85) / (4.2 * 72) = 28.095 mL/min. Hence, the patient's creatinine clearance is 28.095 mL/min. | An 18-year-old adolescent female was evaluated at 15 weeks’ gestation for history of persistent emesis for four weeks, extreme fatigue and red colored urine for one day. There was no history of fever, diarrhea, abdominal pain, or urinary tract infection.
Past medical history was unremarkable for diabetes mellitus, rheumatoid arthritis, or other autoimmune diseases. She was not known to have hyperthyroidism in the past. Pregnancy had been uneventful except for persistent episodes of emesis for past one month. There was no prior history of mood symptoms or altered mental status. There was no history of heat intolerance, diarrhea, or weight loss. There was no recent history of usage of corticosteroid, loop or thiazide diuretic, strenuous exercise, vaginal bleeding, vaginal discharge of grape-like vesicles, seizures, alcohol intake, and carbohydrate load. Family history was notable only for type 2 diabetes in the father. There was no known family history of autoimmune diseases, thyroid disorders, hypokalemia, and periodic paralysis. There was no consanguinity.
Vital signs upon presentation showed blood pressure (BP) 142/87 mm Hg, pulse 120 beats per minute, oral temperature 38.9 °C (102.02 °F), respiratory rate 18 per minute, and oxygen saturation of 97%. Her height was 172.7 cm and weight was 109 kg (240 lb 4.8 oz). Physical examination was remarkable for an overweight female who was awake but slow to respond. There was no goiter and ophthalmopathy. There was mild scleral icterus. There was no tremor or pretibial edema.
Serum beta-human chorionic gonadotropin (hCG) level was 246,000 mIU/mL and sonogram confirmed the presence of a single viable intrauterine fetus of approximately 15 weeks gestation with expected uterine size. Renal function test showed sodium 127 mmol/L, potassium 2.5 mmol/L, bicarbonate 33 mmol/L, blood urea nitrogen (BUN) 123 mg/dL, serum creatinine 4.2 mg/dL (MDRD estimated glomerular filtration rate (eGFR) 17 mL/min/1.73 m2), calcium 9.5 mg/dL, phosphorus 2.7 mg/dL and magnesium of 1 mg/dL. Liver function test showed aspartate aminotransferase 140 IU/L, alanine aminotransferase 203 IU/L, total bilirubin 2.9 mg/dL, ammonia 55 µmol/L, and serum albumin 3.1 gm/dl. Renal function test two months prior to pregnancy showed normal serum creatinine of 0.8 mg/dL (MDRD eGFR 113 mL/min/1.73 m2) and normal electrolytes (serum sodium 138 mmol/L, potassium 3.9 mmol/L, bicarbonate 24 mmol/L, calcium 9.4 mg/dL, phosphorus 3.9 mg/dL, and magnesium was not available) Serum creatine kinase was normal at 121 U/L (normal 0–180 U/L). Urine sodium was <10 mmol/L, urine creatinine 84 mg/dL, urine potassium 28 mmol/L and urine osmolality was 344 mOsm/kg. Fractional excretion of sodium was 0.4%. Urinalysis showed 1+ proteinuria, no microscopic hematuria, 5 white cells per high power field, no ketonuria, pH 5, specific gravity of 1.015, and negative nitrites and leukocytes. Plasma renin activity was 14 ng/mL/h (normal 0.5–4 ng/mL/h, upright) and serum aldosterone was 13 ng/dL (normal 4–31 ng/dL, upright). Blood and urine cultures were negative. Other extensive investigations for infectious etiologies were also negative. Urine for Chlamydia and Neisseria was negative. SARS-CoV-2 DNA PCR from the nasopharyngeal swab was negative. Other labs were notable for undetectable thyroid stimulating hormone (TSH) level < 0.030 mIU/L (reference 0.4–5 mIU/L), total T3 238 ng/dL (reference 87–178 ng/dL), and free T4 > 6.99 ng/dL (reference 0.6–1.2 ng/dL). Computed tomography of the head showed no acute intracranial abnormalities.
Initial management included administration of intravenous fluids (IVF), propranolol, potassium iodide, propylthiouracil (PTU), and hydrocortisone. A presumptive diagnosis of hyperemesis gravidarum with thyroid storm and AKI secondary to persistent emesis was made. She met criteria for thyroid storm due to elevated serum free T4 and total T3 with undetected TSH, along with pyrexia, tachycardia, icterus, and altered mental status. Her clinical condition improved somewhat after receiving PTU, propranolol, and hydrocortisone as heart rate, blood pressure, and free T4 began to decrease. Her mental status improved and she became more alert and engaged in conversation. Given tachycardia and hypertension, she was started on propranolol 60 mg every 4 hours which was later converted to 160 mg daily.
Other thyroid studies showed thyroid peroxidase antibody 0.3 IU/mL (reference < 9 IU/mL), TSH receptor antibody (TRAb) < 0.90 (reference < 1.75 IU/L), and undetected thyroid stimulating immunoglobulin (TSI) of < 0.10 (reference ≤ 0.54 IU/L). Given negative TRAb, Graves’ disease was highly unlikely. Serum free T4 normalized in ten days, TSH in two weeks and total T3 in five days. Given pregnancy, further modalities including radioactive iodine uptake study were not pursued, given risk of fetal hypothyroidism, mental retardation, and increased risk of malignancy. Partial molar pregnancy was initially considered due to presentation of thyroid storm, however, the beta-hCG level was trending down and the patient did not show any signs of pre-eclampsia. Thyroid sonogram showed normal sized thyroid with homogenous thyroid texture and without increased vascularity, making Grave’s disease unlikely. Investigations for AKI included renal sonogram which showed right kidney measuring 12.8 cm in length and left kidney measuring 12.6 cm in length with bilateral normal cortical echogenicity without evidence of hydronephrosis or nephrocalcinosis. Hepatic sonogram showed gallbladder sludge. A chest X-ray was normal without pulmonary edema or cardiomegaly. Electrocardiogram showed normal Q-T interval. Echocardiogram was normal with ejection fraction of 65%. Cardiac enzymes were normal.
PTU was later changed to methimazole as she was no longer in the first trimester of pregnancy and as she demonstrated signs of liver insufficiency. Anti-emetics and IVF were discontinued after few days as the patient was able to tolerate well by mouth. Hydrocortisone was discontinued after two days. Subsequently, propranolol was discontinued along with methimazole, as the beta-hCG mediated hyperemesis was thought to be the likely etiology of thyroid symptoms. Her vital signs, including BPs, remained stable and her thyroid levels returned to normal without anti-thyroid drugs. Serum beta-hCG at discharge was 175,557 mIU/mL. Given decreasing level of hCG without other signs or symptoms of gestational trophoblastic disease, molar pregnancy was unlikely. She was discharged without any thyroid medications.
During the hospitalization, her serum potassium remained around 2.4–2.9 meq/L along with serum bicarbonate 30–38 meq/L despite resolution of emesis. Serum magnesium remained low, as well as with values ranging from 1–1.4 mg/dL. Twenty-four hour urine collection showed a urine calcium of 0.04 mg/kg/day. Random urine calcium to creatinine ratio was also low at 0.005. She required multiple intravenous potassium and magnesium supplements. Discharge serum potassium and magnesium was 3.5 meq/L and 1.2 mg/dL, respectively. She was discharged on magnesium oxide 400 mg daily and potassium chloride 10 meq twice daily. BUN and serum creatinine slowly improved with intravenous hydration. Kidney biopsy was not performed and renal replacement therapy was not required. Discharge BUN and serum creatinine was 15 mg/dL and 0.97 mg/dL (MDRD eGFR 90 mL/min/1.73 m2), respectively. Due to the persistent hypokalemia, alkalosis, hypomagnesemia and hypocalciuria despite resolution of emesis, a genetic testing by next generation sequence analysis was done which showed that the patient was homozygous in the SLCA123 (NM_001126108.2) gene for a known sequence variant designated c.2581C>T (p.Arg861Cys) (Prevention Genetics, Marshfield, WI, USA). No further in vitro functional studies were performed, hence the exact functional implication of this variant was unknown. However, to determine the pathogenicity of this variant, in silico tests were performed using SIFT, PolyPhen-2, FATHMM and MutationTaster. The resulting prediction utilizing these in silico tools was “Pathogenic”. At 37 weeks gestation, a healthy infant of 3.5 kilograms was born vaginally without any perinatal complications. The serum creatinine remained stable at 0.7 mg/dL after delivery (MDRD eGFR 132 mL/min/1.73 m2).
What is the patient's Creatinine Clearance using the Cockroft-Gault Equation in terms of mL/min? You should use the patient's adjusted body weight in kg instead of the patient's actual body weight if the patient is overweight or obese based on their BMI. If the patient's BMI's normal, set their adjusted body weight to the minimum of the ideal body and actual weight. If the patient is underweight, please set their adjusted body weight to their actual body weight.
Creatinine Clearance (Cockcroft-Gault Equation): CrCl = ((140 - age) * adjusted weight * (gender_coefficient)) / (serum creatinine * 72), where the gender_coefficient is 1 if male, and 0.85 if female | |
12 | 2 | Creatinine Clearance (Cockcroft-Gault Equation) | lab test | decimal | pmc-4379326-1 | Extracted | The patient is a 78-year-old male patient with renal disease from 9 years ago (March 2005). He has lived in Semnan, Iran. His medical records were reviewed in October 2014. Laboratory findings in the patient at first were as follows: BUN = 22, Cr = 1.3, weight: 60 kg, height: 166 cm, blood pressure 145/95 mmHg. The patient was treated. The BUN and creatinine levels gradually increased and reached to BUN = 43 and Cr = 4 thirty months after the first referral. All laboratory tests were performed in a medical diagnostic laboratory using the calibrated equipment and common methods. The BUN and creatinine levels were measured by auto analyzer TC-6062 manufactured by Tecom Co, China. Blood pressure was measured by the Riester sphygmomanometer (Germany). At that time he had referred for arteriovenous graft and an arteriovenous fistula made by a surgeon. Six months later he had a functional fistula. Patients were treated with the conventional treatment and Eprex. Specific variables in this case were creatinine and GFR. Blood pressure controlled in the range of 110/80 mmHg. The patient's GFR decreased from 20 to 14 cc/min and his last blood pressure was 140/80 mmHg. The mean serum creatinine level was 3, maximum 4.2 and minimum 1.5. At present, the patient is in stage 4 of CKD and under usual medical treatment. | What is the patient's Creatinine Clearance using the Cockroft-Gault Equation in terms of mL/min? You should use the patient's adjusted body weight in kg instead of the patient's actual body weight if the patient is overweight or obese based on their BMI. If the patient's BMI's normal, set their adjusted body weight to the minimum of the ideal body and actual weight. If the patient is underweight, please set their adjusted body weight to their actual body weight. | {'sex': 'Male', 'age': [78, 'years'], 'weight': [60.0, 'kg'], 'height': [166.0, 'cm'], 'creatinine': [1.3, 'mg/dL']} | 39.744 | 37.757 | 41.731 | The formula for computing Cockcroft-Gault is given by CrCl = ((140 - age) * adjusted weight * (gender_coefficient)) / (serum creatinine * 72), where the gender_coefficient is 1 if male, and 0.85 if female. The serum creatinine concentration is in mg/dL.
The patient's gender is male, which means that the gender coefficient is 1.
The patient is 78 years old.
The concentration of creatinine is 1.3 mg/dL.
The formula for computing the patient's BMI is (weight)/(height * height), where weight is the patient's weight in kg and height is the patient's height in m.
The patient's height is 166.0 cm, which is 166.0 cm * 1 m / 100 cm = 1.66 m. The patient's weight is 60.0 kg. The patient's bmi is therefore 60.0 kg / (1.66 m * 1.66 m) = 21.774 kg/m^2.The patient's BMI is 21.8, indicating they are normal weight.
Because the patient is normal, we take take minimum of the ideal body weight and the patient's body as the patient's adjusted weight for the Cockroft-Gault Equation. Hence, the adjusted body weight is the minimum of the two giving us an adjusted body weight of 60.0 kg.
Using the Cockcroft-Gault equation:
CrCl = ((140 - age) * adjusted weight * gender_coefficient) / (serum creatinine * 72).
Plugging the patient's values gives us ((140 - 78) * 60.0 * 1) / (1.3 * 72) = 39.744 mL/min. Hence, the patient's creatinine clearance is 39.744 mL/min. | The patient is a 78-year-old male patient with renal disease from 9 years ago (March 2005). He has lived in Semnan, Iran. His medical records were reviewed in October 2014. Laboratory findings in the patient at first were as follows: BUN = 22, Cr = 1.3, weight: 60 kg, height: 166 cm, blood pressure 145/95 mmHg. The patient was treated. The BUN and creatinine levels gradually increased and reached to BUN = 43 and Cr = 4 thirty months after the first referral. All laboratory tests were performed in a medical diagnostic laboratory using the calibrated equipment and common methods. The BUN and creatinine levels were measured by auto analyzer TC-6062 manufactured by Tecom Co, China. Blood pressure was measured by the Riester sphygmomanometer (Germany). At that time he had referred for arteriovenous graft and an arteriovenous fistula made by a surgeon. Six months later he had a functional fistula. Patients were treated with the conventional treatment and Eprex. Specific variables in this case were creatinine and GFR. Blood pressure controlled in the range of 110/80 mmHg. The patient's GFR decreased from 20 to 14 cc/min and his last blood pressure was 140/80 mmHg. The mean serum creatinine level was 3, maximum 4.2 and minimum 1.5. At present, the patient is in stage 4 of CKD and under usual medical treatment.
What is the patient's Creatinine Clearance using the Cockroft-Gault Equation in terms of mL/min? You should use the patient's adjusted body weight in kg instead of the patient's actual body weight if the patient is overweight or obese based on their BMI. If the patient's BMI's normal, set their adjusted body weight to the minimum of the ideal body and actual weight. If the patient is underweight, please set their adjusted body weight to their actual body weight.
Creatinine Clearance (Cockcroft-Gault Equation): CrCl = ((140 - age) * adjusted weight * (gender_coefficient)) / (serum creatinine * 72), where the gender_coefficient is 1 if male, and 0.85 if female | |
13 | 2 | Creatinine Clearance (Cockcroft-Gault Equation) | lab test | decimal | pmc-7487712-1 | Extracted | A 23-year-old man presented to hospital with a 2-week history of oedema, frothy urine and lower abdominal pain. This is on a background of ulcerative colitis (UC) for which he was on sulfasalazine. He denied any other regular medications, over the counter medications or herbal supplements. His family history included his mother having IgA nephropathy. He was an occasional smoker and rarely consumed alcohol. He denied illicit drug use. On examination, he was mildly tachycardic (105 beats per minute) and normotensive. He was 180 cm tall and weighed 93 kg. He had mild bilateral pitting oedema to his knees. The rest of his examination was unremarkable. Investigations revealed normal renal function with a creatinine of 75 μmol/L, hypoalbuminaemia with a serum albumin of 15 g/l and urinalysis revealing 3+ protein. His urinary albumin to creatinine ratio (uACR) was 944.9 mg/mmol. His total cholesterol was 8.3 mmol/L. GN, vasculitis, infection and myeloma screen (dsDNA, C3 & C4, anti-PLA-2R, hepatitis B & C serology, serum free light chains and serum protein electrophoresis with immunofixation) were negative, with the exception of a positive atypical perinuclear anti-neutrophil cytoplasmic antibody (p-ANCA). Importantly the myeloperoxidase (MPO) and proteinase 3 (PR3) titres were both < 1 IU/ml. ANCA positivity is most likely explained by our patient’s history of UC where ANCA positivity is reported in 60–80% of patients, with a predominant p-ANCA pattern [].
During preparation for renal biopsy our patient was found to have a prolonged activated partial thromboplastin time (aPTT) of 47 s. This corrected on a mixing study. Factor 12 deficiency (29%) was subsequently identified. Haematology opinion was that this conferred no increase in in vivo bleeding risk.
Renal biopsy was undertaken with LM revealing no morphological abnormality (see Fig. ). IF revealed nonspecific trace glomerular deposits of IgM and C3. MCD was the most likely diagnosis. Our patient was consequently commenced on 75 mg oral prednisone daily.
After 1 month our patient achieved complete remission. He was no longer oedematous, his serum albumin was 33 g/l (from 15 g/L) and uACR was 0.7 mg/mmol (from 944.9 mg/mmol). His prednisone was slowly weaned from 75 mg daily to 50 mg daily for a fortnight and then 25 mg daily for a fortnight. Our patient remained in remission with a serum albumin of 39 g/L, total cholesterol of 6 mmol/L and no albuminuria.
The electron microscopy (EM) report from our patient’s renal biopsy returned 2 months later. This revealed patchy foot process effacement, and mesangial expansion with some deposits suggestive of a mesangiopathic process (see Fig. ).
Our patient then suffered a dramatic relapse with the prednisone dose at 20 mg/day. He reported recurrence of frothy urine, 4 kg of weight gain and proteinuria (on urine dipstick given for home monitoring). His prednisone was increased to 25 mg daily but despite this his oedema worsened and proteinuria persisted. Therefore his prednisone dose was further increased to 75 mg daily to induce remission (see Fig. ).
A complete clinical remission was achieved over the next 2 months with serum albumin improving to 38 g/L and total cholesterol to 6.3 mmol/L. At this stage he was commenced on oral cyclosporin 100 mg BD as a steroid sparing agent given the previous failed attempt to wean steroids. Over the next 5 months our patient’s prednisone dosage was weaned more slowly. At a dose of 10 mg prednisone daily he suffered a second relapse with recurrence of oedema in association with albuminuria and hypoalbuminaemia to his previous levels. His prednisone dose was increased back to 50 mg daily and then 75 mg daily to re-induce remission.
Given his multiple relapses, steroid dependence and initial EM report suggestive of a mesangiopathic process, our patient underwent a second renal biopsy. LM was again normal, however IF found significant mesangial deposits of IgM (2–3+) and C3 (2–3+) (see Figs. and ). IgM nephropathy was then consider a possible diagnosis.
This time our patient took longer to achieve remission, requiring 75 mg prednisone daily and an increase in his cyclosporin dose to 125 mg BD. His prednisone dose was again weaned to 25 mg daily. He also self-ceased his cyclosporin. Our patient was adherent to the recommended prednisone dose as he recognised that without it he would relapse, and he felt further relapses would impact his career progression.
After more than 12 months on prednisone 25 mg daily, and a total of 2 years on continuous corticosteroids, our patient agreed to a slow wean of the corticosteroid dose. Our plan was to use anti-human CD20 (Rituximab) if severe nephrosis recurred. He once again relapsed as soon as his prednisone dose reached 20 mg daily. At this stage his prednisone was increased to 50 mg daily, and he received the first of two planned doses of Rituximab 1 g as an outpatient. He suffered no adverse reactions from the rituximab. During this relapse, his serum albumin reached 10 g/L, 24 h urinary protein was 14.76 g/day and his total cholesterol was 11.5 mmol/L (see Fig. ).
Several days after the rituximab infusion, our patient presented to the Emergency Department with a severe headache, nausea and vomiting. His headache had been progressively worsening since the day prior to his rituximab infusion. There were no focal neurological signs on examination. Computed tomography brain (CTB) and computed tomography angiogram (CTA) revealed a right transverse sinus thrombosis and non-occlusive posterior sagittal sinus thrombosis. We found no evidence of any inherited or acquired thrombophilia with extensive testing (anti-thrombin 3, factor V Leiden, lupus anticoagulant, prothrombin gene mutation, protein C & S, JAK 2 mutation analysis and paroxysmal nocturnal haemoglobinuria assay). He was commenced on therapeutic enoxaparin and bridged to warfarin.
He went on to receive a second dose of rituximab 1-month later. Since then he has remained in complete remission (see Fig. ). His prednisone was weaned over the following 6 months, and his prednisone was ceased. A repeat CTB and CTA showed resolution of the transverse sinus and posterior sagittal sinus thromboses and a decision was made to stop anti-coagulation. | What is the patient's Creatinine Clearance using the Cockroft-Gault Equation in terms of mL/min? You should use the patient's adjusted body weight in kg instead of the patient's actual body weight if the patient is overweight or obese based on their BMI. If the patient's BMI's normal, set their adjusted body weight to the minimum of the ideal body and actual weight. If the patient is underweight, please set their adjusted body weight to their actual body weight. | {'sex': 'Male', 'weight': [93.0, 'kg'], 'height': [180.0, 'cm'], 'creatinine': [75.0, 'µmol/L'], 'age': [23, 'years']} | 166.959 | 158.611 | 175.307 | The formula for computing Cockcroft-Gault is given by CrCl = ((140 - age) * adjusted weight * (gender_coefficient)) / (serum creatinine * 72), where the gender_coefficient is 1 if male, and 0.85 if female. The serum creatinine concentration is in mg/dL.
The patient's gender is male, which means that the gender coefficient is 1.
The patient is 23 years old.
The concentration of creatinine is 75.0 µmol/L. We need to convert the concentration to mg/dL. Let's first convert the mass of creatinine from µmol to mg. The mass of creatinine is 75.0 µmol. To convert 75.0 µmol of creatinine to mol, multiply by the conversion factor 1e-06, giving us 75.0 µmol creatinine * 1e-06 mol/µmol = 7.5e-05 mol creatinine. To convert from mol creatinine to grams, multiply by the molar mass 113.12 g/mol, which will give 7.5e-05 mol creatinine * 113.12 g/mol = 0.008 g creatinine. To convert 0.008 g of creatinine to mg, multiply by the conversion factor 1000.0, giving us 0.008 g creatinine * 1000.0 mg/g = 8.0 mg creatinine. The current volume unit is L and the target volume unit is dL. The conversion factor is 10.0 dL for every unit of L. Our next step will be to divide the mass by the volume conversion factor of 10.0 to get the final concentration in terms of mg/dL. This will result to 8.0 mg creatinine/10.0 dL = 0.8 mg creatinine/dL. The concentration value of 75.0 µmol creatinine/L converts to 0.8 mg creatinine/dL.
The formula for computing the patient's BMI is (weight)/(height * height), where weight is the patient's weight in kg and height is the patient's height in m.
The patient's height is 180.0 cm, which is 180.0 cm * 1 m / 100 cm = 1.8 m. The patient's weight is 93.0 kg. The patient's bmi is therefore 93.0 kg / (1.8 m * 1.8 m) = 28.704 kg/m^2.The patient's BMI is 28.7, indicating they are overweight/obese.
Because the patient is overweight/obese, we use the adjusted body weight formula to get the adjusted weight used for Cockroft-Gault Equation. Shown below is the computation for IBW (ideal body weight).
The patient's gender is Male.
The patient's height is 180.0 cm, which is 180.0 cm * 0.393701 in/cm = 70.866 in.
For males, the ideal body weight (IBW) is calculated as follows:
IBW = 50 kg + 2.3 kg * (height (in inches) - 60)
Plugging in the values gives us 50 kg + 2.3 kg * (70.866 (in inches) - 60) = 74.992 kg.
Hence, the patient's IBW is 74.992 kg.Shown below is the computation for ABW (adjusted body weight).
To compute the ABW value, apply the following formula: ABW = IBW + 0.4 * (weight (in kg) - IBW (in kg)). ABW = 74.992 kg + 0.4 * (93.0 kg - 74.992 kg) = 82.195 kg. The patient's adjusted body weight is 82.195 kg.
Using the Cockcroft-Gault equation:
CrCl = ((140 - age) * adjusted weight * gender_coefficient) / (serum creatinine * 72).
Plugging the patient's values gives us ((140 - 23) * 82.195 * 1) / (0.8 * 72) = 166.959 mL/min. Hence, the patient's creatinine clearance is 166.959 mL/min. | A 23-year-old man presented to hospital with a 2-week history of oedema, frothy urine and lower abdominal pain. This is on a background of ulcerative colitis (UC) for which he was on sulfasalazine. He denied any other regular medications, over the counter medications or herbal supplements. His family history included his mother having IgA nephropathy. He was an occasional smoker and rarely consumed alcohol. He denied illicit drug use. On examination, he was mildly tachycardic (105 beats per minute) and normotensive. He was 180 cm tall and weighed 93 kg. He had mild bilateral pitting oedema to his knees. The rest of his examination was unremarkable. Investigations revealed normal renal function with a creatinine of 75 μmol/L, hypoalbuminaemia with a serum albumin of 15 g/l and urinalysis revealing 3+ protein. His urinary albumin to creatinine ratio (uACR) was 944.9 mg/mmol. His total cholesterol was 8.3 mmol/L. GN, vasculitis, infection and myeloma screen (dsDNA, C3 & C4, anti-PLA-2R, hepatitis B & C serology, serum free light chains and serum protein electrophoresis with immunofixation) were negative, with the exception of a positive atypical perinuclear anti-neutrophil cytoplasmic antibody (p-ANCA). Importantly the myeloperoxidase (MPO) and proteinase 3 (PR3) titres were both < 1 IU/ml. ANCA positivity is most likely explained by our patient’s history of UC where ANCA positivity is reported in 60–80% of patients, with a predominant p-ANCA pattern [].
During preparation for renal biopsy our patient was found to have a prolonged activated partial thromboplastin time (aPTT) of 47 s. This corrected on a mixing study. Factor 12 deficiency (29%) was subsequently identified. Haematology opinion was that this conferred no increase in in vivo bleeding risk.
Renal biopsy was undertaken with LM revealing no morphological abnormality (see Fig. ). IF revealed nonspecific trace glomerular deposits of IgM and C3. MCD was the most likely diagnosis. Our patient was consequently commenced on 75 mg oral prednisone daily.
After 1 month our patient achieved complete remission. He was no longer oedematous, his serum albumin was 33 g/l (from 15 g/L) and uACR was 0.7 mg/mmol (from 944.9 mg/mmol). His prednisone was slowly weaned from 75 mg daily to 50 mg daily for a fortnight and then 25 mg daily for a fortnight. Our patient remained in remission with a serum albumin of 39 g/L, total cholesterol of 6 mmol/L and no albuminuria.
The electron microscopy (EM) report from our patient’s renal biopsy returned 2 months later. This revealed patchy foot process effacement, and mesangial expansion with some deposits suggestive of a mesangiopathic process (see Fig. ).
Our patient then suffered a dramatic relapse with the prednisone dose at 20 mg/day. He reported recurrence of frothy urine, 4 kg of weight gain and proteinuria (on urine dipstick given for home monitoring). His prednisone was increased to 25 mg daily but despite this his oedema worsened and proteinuria persisted. Therefore his prednisone dose was further increased to 75 mg daily to induce remission (see Fig. ).
A complete clinical remission was achieved over the next 2 months with serum albumin improving to 38 g/L and total cholesterol to 6.3 mmol/L. At this stage he was commenced on oral cyclosporin 100 mg BD as a steroid sparing agent given the previous failed attempt to wean steroids. Over the next 5 months our patient’s prednisone dosage was weaned more slowly. At a dose of 10 mg prednisone daily he suffered a second relapse with recurrence of oedema in association with albuminuria and hypoalbuminaemia to his previous levels. His prednisone dose was increased back to 50 mg daily and then 75 mg daily to re-induce remission.
Given his multiple relapses, steroid dependence and initial EM report suggestive of a mesangiopathic process, our patient underwent a second renal biopsy. LM was again normal, however IF found significant mesangial deposits of IgM (2–3+) and C3 (2–3+) (see Figs. and ). IgM nephropathy was then consider a possible diagnosis.
This time our patient took longer to achieve remission, requiring 75 mg prednisone daily and an increase in his cyclosporin dose to 125 mg BD. His prednisone dose was again weaned to 25 mg daily. He also self-ceased his cyclosporin. Our patient was adherent to the recommended prednisone dose as he recognised that without it he would relapse, and he felt further relapses would impact his career progression.
After more than 12 months on prednisone 25 mg daily, and a total of 2 years on continuous corticosteroids, our patient agreed to a slow wean of the corticosteroid dose. Our plan was to use anti-human CD20 (Rituximab) if severe nephrosis recurred. He once again relapsed as soon as his prednisone dose reached 20 mg daily. At this stage his prednisone was increased to 50 mg daily, and he received the first of two planned doses of Rituximab 1 g as an outpatient. He suffered no adverse reactions from the rituximab. During this relapse, his serum albumin reached 10 g/L, 24 h urinary protein was 14.76 g/day and his total cholesterol was 11.5 mmol/L (see Fig. ).
Several days after the rituximab infusion, our patient presented to the Emergency Department with a severe headache, nausea and vomiting. His headache had been progressively worsening since the day prior to his rituximab infusion. There were no focal neurological signs on examination. Computed tomography brain (CTB) and computed tomography angiogram (CTA) revealed a right transverse sinus thrombosis and non-occlusive posterior sagittal sinus thrombosis. We found no evidence of any inherited or acquired thrombophilia with extensive testing (anti-thrombin 3, factor V Leiden, lupus anticoagulant, prothrombin gene mutation, protein C & S, JAK 2 mutation analysis and paroxysmal nocturnal haemoglobinuria assay). He was commenced on therapeutic enoxaparin and bridged to warfarin.
He went on to receive a second dose of rituximab 1-month later. Since then he has remained in complete remission (see Fig. ). His prednisone was weaned over the following 6 months, and his prednisone was ceased. A repeat CTB and CTA showed resolution of the transverse sinus and posterior sagittal sinus thromboses and a decision was made to stop anti-coagulation.
What is the patient's Creatinine Clearance using the Cockroft-Gault Equation in terms of mL/min? You should use the patient's adjusted body weight in kg instead of the patient's actual body weight if the patient is overweight or obese based on their BMI. If the patient's BMI's normal, set their adjusted body weight to the minimum of the ideal body and actual weight. If the patient is underweight, please set their adjusted body weight to their actual body weight.
Creatinine Clearance (Cockcroft-Gault Equation): CrCl = ((140 - age) * adjusted weight * (gender_coefficient)) / (serum creatinine * 72), where the gender_coefficient is 1 if male, and 0.85 if female | |
15 | 2 | Creatinine Clearance (Cockcroft-Gault Equation) | lab test | decimal | pmc-5063890-1 | Extracted | A 27-year-old female presented to the Gout Clinic of Peking Union Medical College Hospital with recurrent arthritis and infertility. Fourteen years before presentation, she noticed protrusion of her right ankle but did not undergo evaluation at a hospital. Eight years before presentation, at age 19, she experienced acute pain and swelling of her right ankle. The pain resolved spontaneously but recurred 6 to 7 times/year, involving the bilateral metatarsophalangeal (MTP) joints, bilateral ankles, and right knee. Her serum urate level (SUA) was elevated to 789 μmol/L. A diagnosis of gout was made, and she was prescribed NSAIDs for pain relief and allopurinol and benzbromarone to lower her urate level. However, she discontinued allopurinol and benzbromarone on her own as these medications triggered acute flares. Five years before presentation, she noticed multiple nodules in her MTP joints, ankles, and fingers. The nodules on her feet interfered with normal walking. She also complained of the inability to conceive after 3 years of attempts. Her age at menarche was 14 years, and her cycles were irregular. She was reported to prefer snacks and fatty food during her childhood. Her father had hypertension. Her grandfather had an SUA level greater than 400 μmol/L but without gout. On physical examination, the patient was generally healthy, with a height of 168 cm and a weight of 55 kg. Her blood pressure was 120/80 mmHg. Cardiac and pulmonary examinations were normal. On abdominal palpation, the liver was enlarged with a normal soft texture. A joint examination revealed multiple nodules on the bilateral MTP1 joints, ankles, and fingers.
A serological examination after overnight fasting revealed a SUA level of 548 μmol/L, serum creatinine (Cr) level of 49 μmol/L, fasting glucose level of 3.6 mmol/L, total triglyceride level of 6.22 mmol/L, and total cholesterol level of 6.60 mmol/L. Her resting lactate level was 7.4 mmol/L. Her 24-h urine urate level was 2.262 mmol/24 h, and her fractional excretion of uric acid (FE-UA) was 2.48 %. Her liver enzymes were normal. The estrogen level and basal body temperature curve were normal for her age and menstrual status. Renal ultrasonography revealed normal kidney size with possible calcium deposits in the bilateral renal medulla. Computed tomography (CT) imaging of her abdomen showed hepatomegaly without nodules. The pelvic ultrasonography and salpingography findings were normal. Serum examinations of her parents and her husband were normal.
Whole blood DNA was extracted from all four family members (the patient, both parents, and her husband) after signing an informed consent form. A genetic study was first conducted with a target gene sequencing approach. A search of the OMIM, NIH, and PubMed databases using the key words “FEMALE,” “GOUT,” and “HYPERLACTACIDEMIA” indicated familial juvenile hyperuricaemic nephropathy, glycogen storage disease type I, and glycogen storage disease type II. Next-generation sequencing was used to sequence each of the exons of the UMOD, RENIN, G6PC, SLC37A4, and GAA genes, as well as two SNP loci (rs2231142 and rs72552713) of ABCG2 found in our previous report of a family including a female with gout.
The genetic sequencing results showed that UMOD, RENIN, SLC37A4, GAA and rs72552713 of ABCG2 were all normal in the patient and her family. Sequencing of the G6PC gene revealed composite heterozygous c.190G>T/c.508C>T mutations in the patient, a heterozygous c.190G>T mutation in her father, and a heterozygous c.508C>T mutation in her mother. The genetic analysis of her husband was normal. The c.190G>T mutation was located on exon 1 and encoded a missense mutation of p.V64L, whereas the c.508C>T mutation was located on exon 4 and encoded a nonsense mutation of p.R170X (Fig. ). Sequencing of 50 healthy females and 100 healthy males at the two loci produced normal results. To our knowledge, the c.190G>T mutation has not been reported in previous literature. | What is the patient's Creatinine Clearance using the Cockroft-Gault Equation in terms of mL/min? You should use the patient's adjusted body weight in kg instead of the patient's actual body weight if the patient is overweight or obese based on their BMI. If the patient's BMI's normal, set their adjusted body weight to the minimum of the ideal body and actual weight. If the patient is underweight, please set their adjusted body weight to their actual body weight. | {'sex': 'Female', 'weight': [55.0, 'kg'], 'height': [168.0, 'cm'], 'creatinine': [49.0, 'µmol/L'], 'age': [27, 'years']} | 122.286 | 116.172 | 128.4 | The formula for computing Cockcroft-Gault is given by CrCl = ((140 - age) * adjusted weight * (gender_coefficient)) / (serum creatinine * 72), where the gender_coefficient is 1 if male, and 0.85 if female. The serum creatinine concentration is in mg/dL.
The patient's gender is female, which means that the gender coefficient is 0.85.
The patient is 27 years old.
The concentration of creatinine is 49.0 µmol/L. We need to convert the concentration to mg/dL. Let's first convert the mass of creatinine from µmol to mg. The mass of creatinine is 49.0 µmol. To convert 49.0 µmol of creatinine to mol, multiply by the conversion factor 1e-06, giving us 49.0 µmol creatinine * 1e-06 mol/µmol = 4.9e-05 mol creatinine. To convert from mol creatinine to grams, multiply by the molar mass 113.12 g/mol, which will give 4.9e-05 mol creatinine * 113.12 g/mol = 0.006 g creatinine. To convert 0.006 g of creatinine to mg, multiply by the conversion factor 1000.0, giving us 0.006 g creatinine * 1000.0 mg/g = 6.0 mg creatinine. The current volume unit is L and the target volume unit is dL. The conversion factor is 10.0 dL for every unit of L. Our next step will be to divide the mass by the volume conversion factor of 10.0 to get the final concentration in terms of mg/dL. This will result to 6.0 mg creatinine/10.0 dL = 0.6 mg creatinine/dL. The concentration value of 49.0 µmol creatinine/L converts to 0.6 mg creatinine/dL.
The formula for computing the patient's BMI is (weight)/(height * height), where weight is the patient's weight in kg and height is the patient's height in m.
The patient's height is 168.0 cm, which is 168.0 cm * 1 m / 100 cm = 1.68 m. The patient's weight is 55.0 kg. The patient's bmi is therefore 55.0 kg / (1.68 m * 1.68 m) = 19.487 kg/m^2.The patient's BMI is 19.5, indicating they are normal weight.
Because the patient is normal, we take take minimum of the ideal body weight and the patient's body as the patient's adjusted weight for the Cockroft-Gault Equation. Hence, the adjusted body weight is the minimum of the two giving us an adjusted body weight of 55.0 kg.
Using the Cockcroft-Gault equation:
CrCl = ((140 - age) * adjusted weight * gender_coefficient) / (serum creatinine * 72).
Plugging the patient's values gives us ((140 - 27) * 55.0 * 0.85) / (0.6 * 72) = 122.286 mL/min. Hence, the patient's creatinine clearance is 122.286 mL/min. | A 27-year-old female presented to the Gout Clinic of Peking Union Medical College Hospital with recurrent arthritis and infertility. Fourteen years before presentation, she noticed protrusion of her right ankle but did not undergo evaluation at a hospital. Eight years before presentation, at age 19, she experienced acute pain and swelling of her right ankle. The pain resolved spontaneously but recurred 6 to 7 times/year, involving the bilateral metatarsophalangeal (MTP) joints, bilateral ankles, and right knee. Her serum urate level (SUA) was elevated to 789 μmol/L. A diagnosis of gout was made, and she was prescribed NSAIDs for pain relief and allopurinol and benzbromarone to lower her urate level. However, she discontinued allopurinol and benzbromarone on her own as these medications triggered acute flares. Five years before presentation, she noticed multiple nodules in her MTP joints, ankles, and fingers. The nodules on her feet interfered with normal walking. She also complained of the inability to conceive after 3 years of attempts. Her age at menarche was 14 years, and her cycles were irregular. She was reported to prefer snacks and fatty food during her childhood. Her father had hypertension. Her grandfather had an SUA level greater than 400 μmol/L but without gout. On physical examination, the patient was generally healthy, with a height of 168 cm and a weight of 55 kg. Her blood pressure was 120/80 mmHg. Cardiac and pulmonary examinations were normal. On abdominal palpation, the liver was enlarged with a normal soft texture. A joint examination revealed multiple nodules on the bilateral MTP1 joints, ankles, and fingers.
A serological examination after overnight fasting revealed a SUA level of 548 μmol/L, serum creatinine (Cr) level of 49 μmol/L, fasting glucose level of 3.6 mmol/L, total triglyceride level of 6.22 mmol/L, and total cholesterol level of 6.60 mmol/L. Her resting lactate level was 7.4 mmol/L. Her 24-h urine urate level was 2.262 mmol/24 h, and her fractional excretion of uric acid (FE-UA) was 2.48 %. Her liver enzymes were normal. The estrogen level and basal body temperature curve were normal for her age and menstrual status. Renal ultrasonography revealed normal kidney size with possible calcium deposits in the bilateral renal medulla. Computed tomography (CT) imaging of her abdomen showed hepatomegaly without nodules. The pelvic ultrasonography and salpingography findings were normal. Serum examinations of her parents and her husband were normal.
Whole blood DNA was extracted from all four family members (the patient, both parents, and her husband) after signing an informed consent form. A genetic study was first conducted with a target gene sequencing approach. A search of the OMIM, NIH, and PubMed databases using the key words “FEMALE,” “GOUT,” and “HYPERLACTACIDEMIA” indicated familial juvenile hyperuricaemic nephropathy, glycogen storage disease type I, and glycogen storage disease type II. Next-generation sequencing was used to sequence each of the exons of the UMOD, RENIN, G6PC, SLC37A4, and GAA genes, as well as two SNP loci (rs2231142 and rs72552713) of ABCG2 found in our previous report of a family including a female with gout.
The genetic sequencing results showed that UMOD, RENIN, SLC37A4, GAA and rs72552713 of ABCG2 were all normal in the patient and her family. Sequencing of the G6PC gene revealed composite heterozygous c.190G>T/c.508C>T mutations in the patient, a heterozygous c.190G>T mutation in her father, and a heterozygous c.508C>T mutation in her mother. The genetic analysis of her husband was normal. The c.190G>T mutation was located on exon 1 and encoded a missense mutation of p.V64L, whereas the c.508C>T mutation was located on exon 4 and encoded a nonsense mutation of p.R170X (Fig. ). Sequencing of 50 healthy females and 100 healthy males at the two loci produced normal results. To our knowledge, the c.190G>T mutation has not been reported in previous literature.
What is the patient's Creatinine Clearance using the Cockroft-Gault Equation in terms of mL/min? You should use the patient's adjusted body weight in kg instead of the patient's actual body weight if the patient is overweight or obese based on their BMI. If the patient's BMI's normal, set their adjusted body weight to the minimum of the ideal body and actual weight. If the patient is underweight, please set their adjusted body weight to their actual body weight.
Creatinine Clearance (Cockcroft-Gault Equation): CrCl = ((140 - age) * adjusted weight * (gender_coefficient)) / (serum creatinine * 72), where the gender_coefficient is 1 if male, and 0.85 if female | |
16 | 2 | Creatinine Clearance (Cockcroft-Gault Equation) | lab test | decimal | pmc-7457258-1 | Extracted | A 31-year-old black Congolese female patient, P3G3, who had a pregnancy of 38 weeks and four days, was transferred from a district hospital to a tertiary facility in Kinshasa, Democratic Republic of Congo, for severe preeclampsia with acute on chronic fetal distress. Her past medical history was notable for eclampsia during her first pregnancy in 2011 and preeclampsia in 2013 during her second pregnancy. She had had two cesarean sections for her pregnancies, and she had her antenatal care for her third pregnancy at a referral hospital. She was diagnosed with preeclampsia during her third pregnancy for which she received 250 mg alpha-methyl-dopa twice a day. During the 30th week of gestation, the patient’s systolic blood pressure became labile, oscillating between 140 and 150 mmHg, despite her antihypertension medication. The patient consulted at a district hospital where she underwent a fetal wellbeing ultrasound which did not find anomalies.
The patient was the 7th of 9 children, and her father was hypertensive. She weighed 72 kg for 155 cm, and upon arrival at the authors’ hospital, her blood pressure was 217/152 mmHg. Her heart rate was 101 bpm, her respiratory rate was 24 cpm, and SpO2 was 96% free air. The patient was in pain, she was lucid and coherent, her palpebral conjunctivae were colored, and she had bilateral pitting edema. The fundus height was at 30 cm, the presentation was cephalic, the fetus was bradycardic at 88 bpm, and there were no signs of genital bleeding. The cervix was median, soft, 80% effaced with a 2 cm dilation. Urine deep stick revealed 3+ proteinuria. She had 1.5 mg/dL of creatinine (normal: 0.5–1.5 mg/dL), 22 mg/dL of urea (normal: 10–50 mg/dL), 15,000 white blood cells/ml, 213,000 platelets/ml and 14 g/dL hemoglobin. Based on these findings, we indicated an emergency cesarean section for acute fetal distress, which resulted in the extraction of a dead infant.
Postoperative suites were marked on day two by decompensated anemia (hemoglobin at 7.8 mg/dL) for which the patient was transfused two units of packed red blood cells. On postoperative day three, the patient presented an abdominal effusion, exacerbation of the bilateral pitting edema, blood pressure increase, hematemesis, melena, petechiae, hematuria, and oliguria. Her blood pressure was 215/120 mmHg and she had signs of renal failure (creatinine = 6.9 mg/dL (normal: 0.84–1.21 mg/dL); urea 132.5 mg/dL (normal: 5–20 mg/dL); hyperkalemia at 6.4 mmol/L (normal: 3.5–5 mmol/L); hyponatremia 109 mmol/L (normal: 136–145 mmol/L); hypocalcemia 0.88 mmol/L (normal: 1.12–1.32 mmol/L)), and signs of hepatic failure (AST 135 IU/L, normal: < 33 IU/L; ALT 325 IU/L, normal: < 33 IU/L; prothrombin ratio 100% (normal: 80–110%). PTT was 39 s (normal: 24–35 s), LDH was 1398 IU/L (normal: 120–280 IU/L), and total bilirubin was 0.35 mg/dL (normal: 0-1 mg/dL)). She equally had neutrophilic leukocytosis at 22,180 cells/mm3 and low platelets at 44,000 cells/mm3. Additionally, schistocytes were identified in the peripheral thin smear.
The team excluded TTP and HELLP syndrome as possible causes of the postpartum microangiopathic hemolytic anemia (MAHA). This decision was based on the history, clinical presentation, and laboratory findings. Atypical hemolytic uremic syndrome was retained as the final diagnosis, and in the absence of anti-complement therapy, the patient underwent four sessions of hemodialysis. Hypertension was treated with Nicardipine, 5 mg/hr. IV with a 2.5 mg/hr. increase every 15 min without exceeding 15 mg/hr., and the goal was to lower the systolic blood pressure below 160 mmHg. Hyperkalemia was corrected with insulin and glucose (10 units of insulin dose with 25 g of glucose per each 1 mmol/L of potassium above the normal). A favorable clinical and biologic evolution was observed, and the patient was released for outpatient follow-up on postoperative day 18 (Figs. , and ).
Laboratory tests could not be obtained more frequently due to their financial burden to the patient and her immediate family. The patient had a normal kidney function at postoperative day 160 (urea 24.2 g/dL, creatinine 0.8 mg/dL) and postoperative day 202 (urea 16.9 g/dL, creatinine 0.8 mg/dL). She did not present new episodes of microangiopathic hemolytic anemia. | What is the patient's Creatinine Clearance using the Cockroft-Gault Equation in terms of mL/min? You should use the patient's adjusted body weight in kg instead of the patient's actual body weight if the patient is overweight or obese based on their BMI. If the patient's BMI's normal, set their adjusted body weight to the minimum of the ideal body and actual weight. If the patient is underweight, please set their adjusted body weight to their actual body weight. | {'sex': 'Female', 'age': [31, 'years'], 'weight': [72.0, 'kg'], 'height': [155.0, 'cm'], 'creatinine': [6.9, 'mg/dL']} | 10.726 | 10.19 | 11.262 | The formula for computing Cockcroft-Gault is given by CrCl = ((140 - age) * adjusted weight * (gender_coefficient)) / (serum creatinine * 72), where the gender_coefficient is 1 if male, and 0.85 if female. The serum creatinine concentration is in mg/dL.
The patient's gender is female, which means that the gender coefficient is 0.85.
The patient is 31 years old.
The concentration of creatinine is 6.9 mg/dL.
The formula for computing the patient's BMI is (weight)/(height * height), where weight is the patient's weight in kg and height is the patient's height in m.
The patient's height is 155.0 cm, which is 155.0 cm * 1 m / 100 cm = 1.55 m. The patient's weight is 72.0 kg. The patient's bmi is therefore 72.0 kg / (1.55 m * 1.55 m) = 29.969 kg/m^2.The patient's BMI is 30.0, indicating they are overweight/obese.
Because the patient is overweight/obese, we use the adjusted body weight formula to get the adjusted weight used for Cockroft-Gault Equation. Shown below is the computation for IBW (ideal body weight).
The patient's gender is Female.
The patient's height is 155.0 cm, which is 155.0 cm * 0.393701 in/cm = 61.024 in.
For females, the ideal body weight (IBW) is calculated as follows:
IBW = 45.5 kg + 2.3 kg * (height (in inches) - 60)
Plugging in the values gives us 45.5 kg + 2.3 kg * (61.024 (in inches) - 60) = 47.855 kg.
Hence, the patient's IBW is 47.855 kg.Shown below is the computation for ABW (adjusted body weight).
To compute the ABW value, apply the following formula: ABW = IBW + 0.4 * (weight (in kg) - IBW (in kg)). ABW = 47.855 kg + 0.4 * (72.0 kg - 47.855 kg) = 57.513 kg. The patient's adjusted body weight is 57.513 kg.
Using the Cockcroft-Gault equation:
CrCl = ((140 - age) * adjusted weight * gender_coefficient) / (serum creatinine * 72).
Plugging the patient's values gives us ((140 - 31) * 57.513 * 0.85) / (6.9 * 72) = 10.726 mL/min. Hence, the patient's creatinine clearance is 10.726 mL/min. | A 31-year-old black Congolese female patient, P3G3, who had a pregnancy of 38 weeks and four days, was transferred from a district hospital to a tertiary facility in Kinshasa, Democratic Republic of Congo, for severe preeclampsia with acute on chronic fetal distress. Her past medical history was notable for eclampsia during her first pregnancy in 2011 and preeclampsia in 2013 during her second pregnancy. She had had two cesarean sections for her pregnancies, and she had her antenatal care for her third pregnancy at a referral hospital. She was diagnosed with preeclampsia during her third pregnancy for which she received 250 mg alpha-methyl-dopa twice a day. During the 30th week of gestation, the patient’s systolic blood pressure became labile, oscillating between 140 and 150 mmHg, despite her antihypertension medication. The patient consulted at a district hospital where she underwent a fetal wellbeing ultrasound which did not find anomalies.
The patient was the 7th of 9 children, and her father was hypertensive. She weighed 72 kg for 155 cm, and upon arrival at the authors’ hospital, her blood pressure was 217/152 mmHg. Her heart rate was 101 bpm, her respiratory rate was 24 cpm, and SpO2 was 96% free air. The patient was in pain, she was lucid and coherent, her palpebral conjunctivae were colored, and she had bilateral pitting edema. The fundus height was at 30 cm, the presentation was cephalic, the fetus was bradycardic at 88 bpm, and there were no signs of genital bleeding. The cervix was median, soft, 80% effaced with a 2 cm dilation. Urine deep stick revealed 3+ proteinuria. She had 1.5 mg/dL of creatinine (normal: 0.5–1.5 mg/dL), 22 mg/dL of urea (normal: 10–50 mg/dL), 15,000 white blood cells/ml, 213,000 platelets/ml and 14 g/dL hemoglobin. Based on these findings, we indicated an emergency cesarean section for acute fetal distress, which resulted in the extraction of a dead infant.
Postoperative suites were marked on day two by decompensated anemia (hemoglobin at 7.8 mg/dL) for which the patient was transfused two units of packed red blood cells. On postoperative day three, the patient presented an abdominal effusion, exacerbation of the bilateral pitting edema, blood pressure increase, hematemesis, melena, petechiae, hematuria, and oliguria. Her blood pressure was 215/120 mmHg and she had signs of renal failure (creatinine = 6.9 mg/dL (normal: 0.84–1.21 mg/dL); urea 132.5 mg/dL (normal: 5–20 mg/dL); hyperkalemia at 6.4 mmol/L (normal: 3.5–5 mmol/L); hyponatremia 109 mmol/L (normal: 136–145 mmol/L); hypocalcemia 0.88 mmol/L (normal: 1.12–1.32 mmol/L)), and signs of hepatic failure (AST 135 IU/L, normal: < 33 IU/L; ALT 325 IU/L, normal: < 33 IU/L; prothrombin ratio 100% (normal: 80–110%). PTT was 39 s (normal: 24–35 s), LDH was 1398 IU/L (normal: 120–280 IU/L), and total bilirubin was 0.35 mg/dL (normal: 0-1 mg/dL)). She equally had neutrophilic leukocytosis at 22,180 cells/mm3 and low platelets at 44,000 cells/mm3. Additionally, schistocytes were identified in the peripheral thin smear.
The team excluded TTP and HELLP syndrome as possible causes of the postpartum microangiopathic hemolytic anemia (MAHA). This decision was based on the history, clinical presentation, and laboratory findings. Atypical hemolytic uremic syndrome was retained as the final diagnosis, and in the absence of anti-complement therapy, the patient underwent four sessions of hemodialysis. Hypertension was treated with Nicardipine, 5 mg/hr. IV with a 2.5 mg/hr. increase every 15 min without exceeding 15 mg/hr., and the goal was to lower the systolic blood pressure below 160 mmHg. Hyperkalemia was corrected with insulin and glucose (10 units of insulin dose with 25 g of glucose per each 1 mmol/L of potassium above the normal). A favorable clinical and biologic evolution was observed, and the patient was released for outpatient follow-up on postoperative day 18 (Figs. , and ).
Laboratory tests could not be obtained more frequently due to their financial burden to the patient and her immediate family. The patient had a normal kidney function at postoperative day 160 (urea 24.2 g/dL, creatinine 0.8 mg/dL) and postoperative day 202 (urea 16.9 g/dL, creatinine 0.8 mg/dL). She did not present new episodes of microangiopathic hemolytic anemia.
What is the patient's Creatinine Clearance using the Cockroft-Gault Equation in terms of mL/min? You should use the patient's adjusted body weight in kg instead of the patient's actual body weight if the patient is overweight or obese based on their BMI. If the patient's BMI's normal, set their adjusted body weight to the minimum of the ideal body and actual weight. If the patient is underweight, please set their adjusted body weight to their actual body weight.
Creatinine Clearance (Cockcroft-Gault Equation): CrCl = ((140 - age) * adjusted weight * (gender_coefficient)) / (serum creatinine * 72), where the gender_coefficient is 1 if male, and 0.85 if female |
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