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{
"Calculator ID": 2,
"Calculator Name": "Creatinine Clearance (Cockcroft-Gault Equation)",
"Category": "lab test",
"Lower Limit": "31.351",
"Note ID": "pmc-8217860-1",
"Note Type": "Extracted",
"Relevant Entities": "{'sex': 'Female', 'age': [61, 'years'], 'weight': [46.0, 'kg'], 'height': [154.0, 'cm'], 'creatinine': [1.3, 'mg/dL']}",
"Row Number": 6,
"Upper Limit": "34.651"
} | medical_problem | 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. | 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. | 33.001 |
{
"Calculator ID": 2,
"Calculator Name": "Creatinine Clearance (Cockcroft-Gault Equation)",
"Category": "lab test",
"Lower Limit": "63.655",
"Note ID": "pmc-6967248-1",
"Note Type": "Extracted",
"Relevant Entities": "{'sex': 'Male', 'weight': [87.0, 'kg'], 'height': [175.0, 'cm'], 'creatinine': [1.39, 'mg/dL'], 'age': [53, 'years']}",
"Row Number": 7,
"Upper Limit": "70.355"
} | medical_problem | 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. | 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. | 67.005 |
{
"Calculator ID": 2,
"Calculator Name": "Creatinine Clearance (Cockcroft-Gault Equation)",
"Category": "lab test",
"Lower Limit": "48.651",
"Note ID": "pmc-6197009-1",
"Note Type": "Extracted",
"Relevant Entities": "{'sex': 'Female', 'weight': [79.0, 'kg'], 'height': [65.0, 'in'], 'creatinine': [1.35, 'mg/dL'], 'age': [51, 'years']}",
"Row Number": 8,
"Upper Limit": "53.773"
} | medical_problem | 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. | 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. | 51.212 |
{
"Calculator ID": 2,
"Calculator Name": "Creatinine Clearance (Cockcroft-Gault Equation)",
"Category": "lab test",
"Lower Limit": "16.536",
"Note ID": "pmc-2547098-1",
"Note Type": "Extracted",
"Relevant Entities": "{'sex': 'Male', 'age': [43, 'years'], 'weight': [115.0, 'kg'], 'height': [198.0, 'cm'], 'creatinine': [691.6, 'µmol/L']}",
"Row Number": 9,
"Upper Limit": "18.276"
} | medical_problem | 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. | 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. | 17.406 |
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} | medical_problem | 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. | 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. | 70.556 |
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} | medical_problem | 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. | 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. | 28.095 |
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} | medical_problem | 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. | 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. | 39.744 |
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} | medical_problem | 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. | 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. | 166.959 |
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} | medical_problem | An 11-year-old girl was admitted to our hospital with microscopic hematuria and nephrotic-range proteinuria detected by school urinary screening. The patient did not have any characteristic features of Fabry’s disease such as angiokeratoma or neuralgia. On admission, her physical examination was unremarkable (body weight 47.4 kg, body height 157.3 cm), and her blood pressure normal (106/60 mmHg). Laboratory investigations revealed hypoproteinemia (serum total protein 5.6 g/dL, serum albumin 2.9 g/dL, serum IgG 318 mg/dL). All other biochemical investigations were within normal limits: blood urea nitrogen 8 mg/dL, serum creatinine 0.43 mg/dL, IgA 111 mg/dL, C3 140 mg/dL (normal 84 – 151 mg/dL), C4 26 mg/dL (normal 17 – 40 mg/dL). Anti-hepatitis B surface antigen, anti-hepatitis C antibody, and anti-nuclear antibody were negative. Urinalysis findings were 3+ for occult blood and 3+ for the dipstick protein reaction; her 24-hour urine protein excretion was 2.5 g. Light microscopy analysis of the initial renal biopsy specimen revealed diffuse mesangial proliferative glomerulonephritis with fibrocellular crescents in 4 of 13 glomeruli (a). Immunofluorescence revealed granular deposits of IgA (3+) and C3 (1+) in the mesangial areas (b), and electron microscopy revealed paramesangial electron-dense deposits. Based on these findings, a diagnosis of severe IgA nephropathy was made. The patient was treated intravenously with three courses of methylprednisolone (20 mg/kg/day) pulse therapy (MPT), followed by 2 years of alternate-day prednisolone (initially 1 mg/kg and then tapered gradually) combined with an angiotensin receptor blocker (telmisartan 1 mg/kg/day). In addition, a tonsillectomy was performed 3 months after MPT. However, microscopic hematuria and mild proteinuria persisted.
At the age of 13 years, the patient was re-admitted for a second renal biopsy to assess the therapeutic effect. All laboratory investigations were within normal limits: serum total protein 6.3 g/dL, serum albumin 4.0 g/dL, blood urea nitrogen 12 mg/dL, serum creatinine 0.44 mg/dL, IgA 108 mg/dL, C3 96 mg/dL, C4 26 mg/dL. Urinalysis revealed a 2+ value for occult blood and a dipstick protein reaction of 2+; the 24-hour urine protein excretion was 0.5 g. Light microscopy analysis of the second renal biopsy specimen revealed focal segmental mesangial proliferative glomerulonephritis. Immunofluorescence revealed granular deposits of IgA (2+) and C3 (1+) in the mesangial areas, and electron microscopy revealed paramesangial electron-dense deposits. After the second renal biopsy, the patient was additionally treated with three courses of MPT, and her microscopic hematuria disappeared within 6 months.
At the age of 15 years, she was admitted for a third renal biopsy. On admission, her physical examination was unremarkable (body weight 55.9 kg, body height 165 cm), and her blood pressure normal (102/70 mmHg). Laboratory investigations were all within normal limits: serum total protein 6.6 g/dL, serum albumin 4.2 g/dL, blood urea nitrogen 11 mg/dL, serum creatinine 0.48 mg/dL, IgA 135 mg/dL, C3 121 mg/dL, C4 25 mg/dL. Urinalysis was negative for occult blood and the dipstick protein reaction was 2+; her 24-hour urine protein excretion was 0.7 g. Light microscopy analysis of the third renal biopsy specimen revealed minor glomerular abnormalities (a). Immunofluorescence revealed granular deposits of IgA (2+) in the mesangial areas, and electron microscopy revealed paramesangial electron-dense deposits. In addition, numerous myelin-like bodies were first observed in podocytes (b). Low serum α-galactosidase A activity (13.8 Agal U, cut-off value < 20) and increased GL3 excretion in the urine (0.54 mg/mgCr, control 0.1 – 0.4) were also observed. On the basis of these findings, a final diagnosis of concomitant IgA nephropathy (healing stage) and subclinical Fabry’s disease was made. | 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. | 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 15 years old.
The concentration of creatinine is 0.48 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 165.0 cm, which is 165.0 cm * 1 m / 100 cm = 1.65 m. The patient's weight is 55.9 kg. The patient's bmi is therefore 55.9 kg / (1.65 m * 1.65 m) = 20.533 kg/m^2.The patient's BMI is 20.5, 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 55.9 kg.
Using the Cockcroft-Gault equation:
CrCl = ((140 - age) * adjusted weight * gender_coefficient) / (serum creatinine * 72).
Plugging the patient's values gives us ((140 - 15) * 55.9 * 0.85) / (0.48 * 72) = 171.857 mL/min. Hence, the patient's creatinine clearance is 171.857 mL/min. | 171.857 |
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} | medical_problem | 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. | 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. | 122.286 |
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} | medical_problem | 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. | 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. | 10.726 |
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} | medical_problem | A 32-year-old male patient was admitted to the outpatient clinic with complaints of weight gain, dry mouth, and fatigue. In 2002, some eruptions appeared on the skull. Two (2) years later, skin eruptions spread all over his body. At that time, he was diagnosed with psoriasis and prescribed topical clobetasol propionate. He had not been reexamined after that and has been using clobetasol propionate 0.005% routinely for 10 years. He has applied the drug to his arms, legs, and all over the trunk. Over the past year, he put on weight obviously (8 kg). He stopped the treatment 1 month ago, at the time of writing. He has been complaining of dry mouth and fatigue for the last month. On his physical examination, moon face, central adiposity, and purple-red striae on the abdomen under umbilicus were observed. There were scaly patches and erythematous plaques on the skull, interscapular area, sacrum, arms, legs, knees, and elbows []. Other systemic examinations were all normal. Blood pressure was 130/90 mmHg, pulse 75/min, height 1.76 m, weight 77 kg, and body mass index 24.8 kg/m2. On laboratory examination, fasting blood glucose: 152 mg/dL (N: 70-105), creatinine: 1 mg/dL (N: 0.72-1.25), triglyceride: 160 mg/dL (N: 0-200), total cholesterol: 240 mg/dL (N: 0-200), high-density-lipoprotein (HDL)-cholesterol: 44 mg/dL (N: 45-55), low-density-lipoprotein (LDL)-cholesterol: 164 mg/dL (N: 0-130), ALT: 42 u/L (N: 0-55); AST: 27 u/L (N: 0-34); sodium: 140 mmol/L (N: 136-145); potassium: 4.6 mmol/L (N: 3.5-5.1); calcium: 9.9 mg/dL (N: 8.4-10.2); phosphorus: 3.5 mg/dL (N: 2.3-4.7); albumin: 4.6 g/dL (N: 3.2-5.2); intact-parathyroid hormone (iPTH): 38 pg/mL (N: 14-72); 25-OH Vitamin D: 4.9 ng/mL (N: 24-50); white blood cell (WBC) count: 12.76-103 /uL (N: 4.23-9.07); hemoglobin (Hb) count: 14.7 gr/dL (N: 13.7-17.5); platelet: 217-103 /uL (N: 150-400); morning (8 AM) adrenocorticotropic hormone (ACTH): 5.6 pg/mL (N: 0-46); morning (8 AM) serum cortisol: <0.2 μg/dL (5.5 nmol/L) (N: 4.3-22.4). According to these findings, the patient was diagnosed with iatrogenic Cushing's syndrome secondary to topical steroid use. For adrenal insufficiency, 20 mg/day hydrocortisone treatment was commenced, and for vitamin D deficiency, vitamin D replacement. As the patient had high blood glucose levels, dyslipidemia, and large waist circumference (101 cm), he was diagnosed with metabolic syndrome, and a low-calorie diet and exercise were advised. Metformin treatment at a dose of 2000 mg/day was commenced for glucose regulation. The patient consulted at the dermatology department for his psoriasis, and calcipotriol pomade and emollients were prescribed. One (1) month after that, 1 μg tetracosactide i.v. was applied and cortisol levels were measured at 30 min and at 60 min. As both measured levels were below 3 μg/dL, glucocorticoid maintenance treatment was continued. | 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. | 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 32 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 1.76 m. The patient's weight is 77.0 kg. The patient's bmi is therefore 77.0 kg / (1.76 m * 1.76 m) = 24.858 kg/m^2.The patient's BMI is 24.9, 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 71.369 kg.
Using the Cockcroft-Gault equation:
CrCl = ((140 - age) * adjusted weight * gender_coefficient) / (serum creatinine * 72).
Plugging the patient's values gives us ((140 - 32) * 71.369 * 1) / (1.0 * 72) = 107.053 mL/min. Hence, the patient's creatinine clearance is 107.053 mL/min. | 107.053 |
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} | medical_problem | The patient is a 28-year-old Hispanic female with a past medical history of
hypertension, high serum cholesterol, and gastritis who presented to the emergency
room for the evaluation of abdominal pain of 2 days duration. Six months prior, she
had similar pain. An upper gastrointestinal (GI) endoscopy at that time showed
peptic ulcer disease and no other mucosal lesions. The patient had a strong family
history of renal disease and 2 of her siblings required a renal transplant, but she
did not know what kidney pathology they had. Her medications included Lisinopril
oral 10 mg tablet daily and Pantoprazole oral 40 mg daily. On presentation at the
emergency room (ER), her height and weight were 157 cm and 61 kg, respectively, and
her blood pressure was 206/121 mm Hg. On physical examination, the patient had
epigastric tenderness. The rest of her physical examination was unremarkable.
Radiology was ordered to exclude any anatomical abnormality. A computed tomography
scan showed neither atrophy nor enlargement of the kidneys. She then followed up as
an outpatient with a nephrologist shortly after her ER visit. Her laboratory work up
during that visit revealed the following: nephrotic range proteinuria (9.2 g protein
on 24-hour urine collection; reference range, 0-2.5 g/d), hypoalbuminemia (300
µmol/L; reference range, 421-662 µmol/L), hypoproteinemia (50 g/L; reference range,
60-80 g/L), elevated serum creatinine (148.5 µmol/L; reference range, 44-80 μmol/L),
high chloride (110 mmol/L; reference range, 98-106 mmol/L), and low hemoglobin (100
g/L; reference range, 120-160 g/L). The lipid profile showed an increased total
cholesterol level (8.3 mmol/L; reference range, <5.2 mmol/L), elevated
triglycerides (3.7 mmol/L; reference range, <1.70 mmol/L), elevated low-density
lipoprotein fraction (5.9 mmol/L; reference range, <2.6 mmol/L), and decreased
high-density lipoprotein fraction (1.1 mmol/L; reference range, ≥1.55 mmol/L). After
treating her blood pressure, the patient underwent a US-guided renal biopsy. | 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. | 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 28 years old.
The concentration of creatinine is 148.5 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 148.5 µmol. To convert 148.5 µmol of creatinine to mol, multiply by the conversion factor 1e-06, giving us 148.5 µmol creatinine * 1e-06 mol/µmol = 0.000149 mol creatinine. To convert from mol creatinine to grams, multiply by the molar mass 113.12 g/mol, which will give 0.000149 mol creatinine * 113.12 g/mol = 0.017 g creatinine. To convert 0.017 g of creatinine to mg, multiply by the conversion factor 1000.0, giving us 0.017 g creatinine * 1000.0 mg/g = 17.0 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 17.0 mg creatinine/10.0 dL = 1.7 mg creatinine/dL. The concentration value of 148.5 µmol creatinine/L converts to 1.7 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 157.0 cm, which is 157.0 cm * 1 m / 100 cm = 1.57 m. The patient's weight is 61.0 kg. The patient's bmi is therefore 61.0 kg / (1.57 m * 1.57 m) = 24.747 kg/m^2.The patient's BMI is 24.7, 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 49.665 kg.
Using the Cockcroft-Gault equation:
CrCl = ((140 - age) * adjusted weight * gender_coefficient) / (serum creatinine * 72).
Plugging the patient's values gives us ((140 - 28) * 49.665 * 0.85) / (1.7 * 72) = 38.628 mL/min. Hence, the patient's creatinine clearance is 38.628 mL/min. | 38.628 |
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} | medical_problem | A 73-yr-old woman with atrial fibrillation presented to the emergency room complaining of chest discomfort, dyspnea, and agitation. The patient had suffered from atrial fibrillation for the last 2 yr. Her medications for the previous 2 yr included diltiazem 90 mg, metoprorol 25 mg, and aspirin 100 mg twice a day. In addition, she had been taking mirtazapine 30 mg, alprazolam 0.25 mg, and zolpidem 10 mg daily for a 6 yr history of dysthymia.
Physical examination showed a blood pressure of 100/83 mmHg, a heart rate of 100 beats/min, and a normal body temperature. Her body weight was 62.3 kg, and she was 158 cm in height. Initial laboratory results were unremarkable with a normal PT of 12.3 sec (INR 1.0). Routine chemical studies indicated normal values for total protein (6.6 g/dL), albumin (3.9 g/dL), aspartate aminotransferase (17 U/L), alanine aminotransferase (10 U/L), alkaline phosphatase (79 U/L), total bilirubin (0.3 mg/dL) blood urea nitrogen (16.4 mg/dL), creatinine (0.6 mg/dL), and electrolytes. Results of hematological studies including complete blood counts were also normal. Mild cardiomegaly was found on the chest radiography. Electrocardiogram showed atrial fibrillation. Echocardiogram revealed mild aortic, mitral, and tricuspid regurgitation and left atrial enlargement (45 mm).
The patient underwent heparinization with an initial bolus administration of 3,600 IU heparin followed by continuous infusion for 6 days. Then the patient was started on 2 or 3 mg of warfarin daily (16.3 mg/week) to prevent thromboembolism, and was discharged after 3 days with a PT of 37.4 sec (INR 2.81). When she revisited the outpatient clinic after 3 days, her PT was found to be 50.0 sec (INR 3.68). After normalization of the patient's PT with warfarin withdrawal for 3 days, 1 or 2 mg/day (10.5 mg/week) of warfarin was prescribed. The PT after 3 days of treatment was 41.6 sec (INR 3.11). The administration of warfarin dose was changed (6.5-10.5 mg/week) continuously, which resulted in a PT of 20.9-43.1 sec (INR 1.64-3.21). She had to discontinue warfarin therapy temporarily 3 times. The difficulty in finding the optimal treatment dose during the induction period of anticoagulation continued for more than 2 month.
The patient continues to receive warfarin therapy at the outpatient clinic monthly and her PT remains within the recommended target therapeutic range (INR 2.0-3.0), even though her warfarin dose has been reduced to 6.5 mg/week.
The patient was genotyped for CYP2C9 after informed consent. DNA was isolated from peripheral blood, and all 9 exons of the CYP2C9 gene were amplified by PCR (-). The PCR products were sequenced using the ABI PRISIM BigDye terminator Cycle sequencing kit and an ABI Prism 3100 Genetic Analyzer (Applied Biosystems, Foster City, CA, U.S.A.). The patient was found to be an intermediate metabolizer with the genotype of CYP2C9*3/*4 (). | 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. | 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 73 years old.
The concentration of creatinine is 0.6 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 158.0 cm, which is 158.0 cm * 1 m / 100 cm = 1.58 m. The patient's weight is 62.3 kg. The patient's bmi is therefore 62.3 kg / (1.58 m * 1.58 m) = 24.956 kg/m^2.The patient's BMI is 25.0, 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 158.0 cm, which is 158.0 cm * 0.393701 in/cm = 62.205 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 * (62.205 (in inches) - 60) = 50.571 kg.
Hence, the patient's IBW is 50.571 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 = 50.571 kg + 0.4 * (62.3 kg - 50.571 kg) = 55.263 kg. The patient's adjusted body weight is 55.263 kg.
Using the Cockcroft-Gault equation:
CrCl = ((140 - age) * adjusted weight * gender_coefficient) / (serum creatinine * 72).
Plugging the patient's values gives us ((140 - 73) * 55.263 * 0.85) / (0.6 * 72) = 72.852 mL/min. Hence, the patient's creatinine clearance is 72.852 mL/min. | 72.852 |
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} | medical_problem | We are presenting a case with acute abdomen, i.e. ileoileal intusussception, caused by Burkitt lymphoma. A sixteen-year-old Caucasian Kosovar boy, presented in the surgical emergency clinic as acute abdomen, with abdominal pain, nausea, vomiting, and problems with defecation and flatulence. The symptoms started three days ago, worsening on admission day.
The patient's height was 178 cm, and his weight was 70 kg. His vital signs were: blood pressure 120/80 mmHg; pulse rate: 76 beats/min; respiratory rate 20/min; body temperature 37.1°C.
During physical examination, a distended, diffusely tender and painful abdomen with lower abdomen rebound was revealed. The patient's skin was pale with sweats.
Plane abdominal radiography showed mechanical obstruction. (Fig. )
The emergency laboratory tests presented as follows: Red blood cells (RBC): 4.61 × 109/L; white blood cells (WBC): 7.3 × 109/L; Hemoglobin (Hgb): 128 g/L; Hematocrit (Htc): 0.42; blood sugar: 5.42 mmol/L; blood urea nitrogen (BUN): 2.6 mmol/L; serum creatinine: 88 μmol/L; BUN/Creat ratio: 8.5; total protein: 72 g/L; albumin: 36 g/l; ALP: 60 IU/L; ALT: 26 IU/L; AST:40 IU/L; direct bilirubin: 5.8 μmol/L; total bilirubin: 20.5 μmol/L; indirect bilirubin: 14.7 μmol/L; Gama GT: 26 IU/L; C-reactive protein: 15.6 mg/L; serum amylase: 30 U/L: electrolytes: Na: 138 mmol/L; K: 3.75 mmol/L; Cl: 102 mmol/L; urinalysis: 2-4 Leucocytes, some bacteria and some uric acid crystals. Blood group: O Rh(D) poz.
Three weeks prior he had been surgically treated as acute abdomen caused by acute appendicitis and Mckelly Diverticulitis. Appendectomy and short resection of the ileum with diverticulum, and end-to-end anastomosis was performed. The immediate post operative period went well. After his discharge, his second hospital admission was two weeks after operation with abdominal pain and constipation problems which released spontaneously after two days.
At his third admission as acute abdomen, urgent laparotomy was performed in general endo tracheal anesthesia on the day after admission. Intra operative findings revealed small bowel dilatation, with intussusceptions of the terminal ileum, 2 cm from ileocecac valve. There were multiple enlarged mesenteric lymph nodes at the meso of the terminal ileum, ascending and the transverse colon, without palpable liver metastases.
We have done des intussusceptions caused by tumor from the wall of the ileum. (Fig. , , )
Adhesions at the anastomosis, and 60 cm above that, were released. The right extended haemicolectomy with end to end ileum-transverse anastomosis was performed. Post operative period went well; blood pressure was 120/80 mmHg, pulse rate beats: 65/min; temp.: 36.7°C. The wound healed per primam. He was treated with frozen fresh plasma (several doses-seven), red blood cells (one dose); antibiotic, analgesics, H2 blockers, vitamins, amino acids, human albumins. He was discharged on the 10th postoperative days, with good bowel movements. He was oriented to the Hematology Department for further treatment, for Burkitt Lymphoma with chemotherapy.
HP opinion: Giemsa staining demonstrated neoplastic lymphocytes infiltration. Immunochemical testing was positive for Burkitt lymphoma (CD10, CD20, CD34, Bcl-2, Ki67, IgM, MIB-1 with a proliferation index of over 90% of neoplastic cells) and c-myc translocation determined by FISH analysis (fusion and split). (Fig. , , , , ) | 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. | 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 16 years old.
The concentration of creatinine is 88.0 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 88.0 µmol. To convert 88.0 µmol of creatinine to mol, multiply by the conversion factor 1e-06, giving us 88.0 µmol creatinine * 1e-06 mol/µmol = 8.8e-05 mol creatinine. To convert from mol creatinine to grams, multiply by the molar mass 113.12 g/mol, which will give 8.8e-05 mol creatinine * 113.12 g/mol = 0.01 g creatinine. To convert 0.01 g of creatinine to mg, multiply by the conversion factor 1000.0, giving us 0.01 g creatinine * 1000.0 mg/g = 10.0 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 10.0 mg creatinine/10.0 dL = 1.0 mg creatinine/dL. The concentration value of 88.0 µmol creatinine/L converts to 1.0 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 178.0 cm, which is 178.0 cm * 1 m / 100 cm = 1.78 m. The patient's weight is 70.0 kg. The patient's bmi is therefore 70.0 kg / (1.78 m * 1.78 m) = 22.093 kg/m^2.The patient's BMI is 22.1, 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 70.0 kg.
Using the Cockcroft-Gault equation:
CrCl = ((140 - age) * adjusted weight * gender_coefficient) / (serum creatinine * 72).
Plugging the patient's values gives us ((140 - 16) * 70.0 * 1) / (1.0 * 72) = 120.556 mL/min. Hence, the patient's creatinine clearance is 120.556 mL/min. | 120.556 |
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} | medical_problem | A 70-year-old man comes to the emergency room for worsening leg pain and a rash consistent with wet gangrene. He has no history of skin infections but has type 2 diabetes mellitus and has smoked 2 packs of cigarettes daily for 20 years. Three days after admission, he becomes increasingly hypoxic and tachypneic. He is emergently intubated and ventilatory support is initiated. He is 180 cm (5 ft 11 in) tall and weighs 90 kg (198 lb); BMI is 27.8 kg/m2. His pulse is 112/min and his blood pressure is 95/60 mmHg. The ventilator is set at an FIO2 of 100%, tidal volume of 540 mL, respiratory rate of 20/min, and positive end-expiratory pressure (PEEP) of 5 cm H2O. On pulmonary examination, there are diffuse crackles. Cardiac examination shows no abnormalities. Hemoglobin is 11.5 g/dL, serum lactate is 4.0 mmol/L, and serum creatinine is 2.5 mg/dL. An arterial blood gas checked 30 minutes after intubation shows a PaCO2 of 50 mm Hg and a PaO2 of 55 mm Hg. An x-ray of the chest shows new bilateral infiltrates. | 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. | 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 70 years old.
The concentration of creatinine is 2.5 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 180.0 cm, which is 180.0 cm * 1 m / 100 cm = 1.8 m. The patient's weight is 90.0 kg. The patient's bmi is therefore 90.0 kg / (1.8 m * 1.8 m) = 27.778 kg/m^2.The patient's BMI is 27.8, 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 * (90.0 kg - 74.992 kg) = 80.995 kg. The patient's adjusted body weight is 80.995 kg.
Using the Cockcroft-Gault equation:
CrCl = ((140 - age) * adjusted weight * gender_coefficient) / (serum creatinine * 72).
Plugging the patient's values gives us ((140 - 70) * 80.995 * 1) / (2.5 * 72) = 31.498 mL/min. Hence, the patient's creatinine clearance is 31.498 mL/min. | 31.498 |
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} | medical_problem | A 35-year-old man diagnosed with type 2 diabetes (T2D) eight years ago and treated with intermittent metformin administration visited our clinic. He had a history of a spontaneously healed ureteral stones ten years ago. He was 169.3 cm tall, weighed 51.6 kg, and his body mass index (BMI) was 18 kg/m2. None of his family members had a known history of diabetes. He complained of a warm and painful lesion on his thigh for the last three weeks, but reported no recent history of trauma or injection. Initial physical examination of the painful lesion revealed tenderness and non-pitting edema of the anteromedial right thigh. His blood pressure and body temperature were 120/80 mmHg and 36.4℃, respectively. There was no leukocytosis (white blood cell count: 9,190/µL) and C-reactive protein was normal, but the erythrocyte sedimentation rate was elevated to 62 mm/hr. His glycemic control was very poor, with an HbA1c 14.5% and postprandial glucose of 446 mg/dL. Other biochemistry values were as follows: serum creatinine 0.4 mg/dL, blood urea nitrogen 24 mg/dL, potassium 4.6 mmol/L, sodium 132 mmol/L, calcium 9.1 mg/dL, phosphorus 3.6 mg/dL, alkaline phosphatase 86 U/L, albumin 4.1 g/dL, and creatinine kinase 436 mg/dL. He had proteinuria (trace) and glycosuria (4+) on urinalysis.
Serial blood culture showed no evidence of bacterial infection. As infectious causes were thought to be less likely, we conducted arterial and venous doppler ultrasonography of the extremity to exclude vascular problems such as deep vein thrombosis or peripheral artery disease. There was no evidence of vascular structural abnormality, but an ill-defined hyperechoic lesion and thick fluid collection in the right vastus medialis muscle was found. After four days, the amount of fluid increased, and thus fluid aspiration at the intermuscular fascial plane adjacent to the vastus lateralis was done (). The fluid was clear, watery and serous. Gram stain and culture of the fluid were negative. Magnetic resonance image (MRI) of the right thigh reflected diffuse edema around the vastus medialis with low signal intensity on T1 () and high signal intensity on T2 images (). The three-phase bone scan showed increased blood flow to the right thigh consistent with myonecrosis as shown on the thigh MRI (). The bone scan also revealed increased blood flow at the right medial tibial condyle consistent with an insufficiency fracture, which was subsequently confirmed by X-ray and MRI (). Since these clinical findings and images were highly suggestive of DMI of the right vastus medialis with insufficient fracture of the right tibial condyle, a muscle biopsy was not performed.
Due to the early onset of disease (age 27), no obesity and no family history of T2D, we needed to clearly identify the exact type of his diabetes. Baseline C-peptide level was very low (0.1 ng/mL) and did not sufficiently rise at 6 min after glucagon stimulation test (0.3 ng/mL). Antinuclear antibodies, and anti-IA2 antibody results were not significant, but antibodies to glutamic acid decarboxylase (anti-GAD Ab) were positive (2.0 U/mL). Other immunologic factors were negative. Considering his age, low BMI, positive anti-GAD Ab, and severely decreased C-peptide level, we diagnosed his diabetes as a case of latent autoimmune diabetes in adults (LADA). After we examined microvascular and macrovascular diabetic complications, he was diagnosed with peripheral neuropathy and non-proliferative retinopathy of both eyes as well as microalbuminuria based on spot urine analysis (152 µg/mg Creatinine).
When we evaluated the cause of the insufficiency fracture, we found that his bone mineral density (BMD) was reduced, with T-scores of -3.9 (Z-score -3.3) at L1-L4 and -2.7 (Z-score -2.3) at the femur neck. Due to the young age of the patient, we also evaluated possible etiologies of secondary osteoporosis, including hyperparathyroidism, hyperthyroidism, hypogonadism, and glucocorticoid excess. 25-hydroxy-vitamin D (25-[OH]D) level was also lower than the normal limits (<4 ng/mL, normal range 11.1 to 42.9) and osteocalcin level was slightly decreased (2.4 ng/mL, normal range 2.7 to 11.5). Thyroid function test was normal (free-T4 0.90 ng/dL, normal range 0.77 to 1.94 ng/dL; Thyroid stimulating hormone 2.24 µU/mL, normal range 0.30 to 4.00 µU/mL; T3 120 ng/dL, normal range 80 to 200 ng/dL), and there was no significant finding of thyroid autoantibodies. Parathyroid hormone (PTH) level was 19.6 pg/mL (normal range 13 to 54 pg/mL). C-telopeptide level was within normal limits (0.74 ng/mL, normal range 0.07 to 0.78 ng/mL). Testosterone and follicle stimulating hormone (FSH) levels were also within normal limits (Testosterone 2.19 ng/mL, normal range, 1.8 to 8.96 ng/mL; FSH 4.0 ng/mL, normal range, 2.8 to 9.6 ng/mL), with a slightly low luteinizing hormone level (1.3 ng/mL, normal range, 1.8 to 5.2 ng/mL).
Antibiotics were initially prescribed, but discontinued when bacterial infection was ruled out and DMI was thought to be the most likely clinical diagnosis. Instead, the patient was treated with analgesics such as acetaminophen, application of a long leg splint and bed rest, and multiple daily injections of insulin for strict glucose control. For his osteoporotic fracture, he was administered oral vitamin D and calcium agents. After about two weeks of supportive management, the tenderness and swelling of the right anteromedial thigh gradually reduced and the patient was able to walk without help, and so the splint was removed. 3 months later, when the hyperglycemia was controlled, we have done the oral glucose tolerance test and calculated the insulinogenic index (IGI, delta insulin 30 min-0 min/delta glucose 30 min-0 min). Calculated IGI was 0 (reference range >0.5), which reflects diminished beta-cell function on glucose stimulation. On follow-up ultrasonography after 6 months, the myonecrosis of the right vastus medialis muscle was dramatically resolved and his HbA1c had improved to 5.7%. In addition, his 25-(OH)D level had risen to 58.7 ng/mL after 6 months of treatment. Five months after treatment, the patient complained of frequent injections, so we changed his insulin regimen to a premixed combination insulin injection twice a day. He is currently under follow-up at the outpatient clinic without any evidence of recurrence. | 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. | 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 35 years old.
The concentration of creatinine is 0.4 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 169.3 cm, which is 169.3 cm * 1 m / 100 cm = 1.693 m. The patient's weight is 51.6 kg. The patient's bmi is therefore 51.6 kg / (1.693 m * 1.693 m) = 18.003 kg/m^2.The patient's BMI is 18.0, indicating they are underweight.
Because the patient is underweight, we take the patient's weight, 51.6 kg as the patient's adjusted weight needed for the Cockroft-Gault Equation.
Using the Cockcroft-Gault equation:
CrCl = ((140 - age) * adjusted weight * gender_coefficient) / (serum creatinine * 72).
Plugging the patient's values gives us ((140 - 35) * 51.6 * 1) / (0.4 * 72) = 188.125 mL/min. Hence, the patient's creatinine clearance is 188.125 mL/min. | 188.125 |
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} | medical_problem | A 58-year-old patient comes to the physician because of progressive pain and swelling of his left calf for the past 2 days. He has no personal or family history of serious illness. He does not smoke or drink alcohol. His last digital rectal examination and colonoscopy at the age of 50 years were normal. His vital signs are within normal limits. He is 183 cm (6 ft) tall and weighs 80 kg (176 lb); BMI is 24 kg/m2. Physical examination shows redness, warmth, and tenderness of the left calf. The circumference of the left lower leg is 4 cm greater than the right. Dorsiflexion of the left foot elicits pain in the ipsilateral calf. Laboratory studies show:
Hemoglobin 15 g/dL
Leukocyte count 9000/mm3
Platelet count 190,000/mm3
Erythrocyte sedimentation rate 12 mm/h
Serum
Urea nitrogen 18 mg/dL
Creatinine 1.0 mg/dL
Alkaline phosphatase 24 U/L
Aspartate aminotransferase (AST, GOT) 12 U/L
Alanine aminotransferase (ALT, GPT) 10 U/L
Urine
Protein negative
RBC 1/hpf
WBC none
Compression ultrasonography with Doppler shows a non-compressible left popliteal vein with a visible 0.5-cm hyperechoic mass and reduced flow. | 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. | 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 58 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 183.0 cm, which is 183.0 cm * 1 m / 100 cm = 1.83 m. The patient's weight is 80.0 kg. The patient's bmi is therefore 80.0 kg / (1.83 m * 1.83 m) = 23.888 kg/m^2.The patient's BMI is 23.9, 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 77.708 kg.
Using the Cockcroft-Gault equation:
CrCl = ((140 - age) * adjusted weight * gender_coefficient) / (serum creatinine * 72).
Plugging the patient's values gives us ((140 - 58) * 77.708 * 1) / (1.0 * 72) = 88.501 mL/min. Hence, the patient's creatinine clearance is 88.501 mL/min. | 88.501 |
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} | medical_problem | A 43-year old male presented with a history of proteinuria discovered on a routine medical examination in 1985 when he was 22 years old. His medical history was acute pancreatitis at age 17 and hypertension at age 40, and the family history indicated that his nephew had IgA nephropathy. The patient occasionally consumes alcohol, but doesn’t smoke. The patient visited a local doctor and underwent a renal biopsy for suspected active nephritis because of the finding (Table ) of hematuria 3+ protein from pooled urine 0.78 g/day and a plasma creatinine (Cr) level of 1.16 mg/dl [estimated glomerular filtration rate (eGFR) 71 ml/min/1.73 m2]. Pathologic examination revealed IgA nephropathy with partial cellular crescent formation in 1 of the 12 glomeruli, slight mesangial matrix expansion, and mild atrophy of the renal tubule and interstitium. He was followed up without treatment, and the urinary abnormalities resolved spontaneously. He stopped visiting the hospital 3 years after the first visit because of the repeated negative urine analysis and did not visit any other hospital thereafter. He continued to undergo routine medical examinations, which were intermittently positive for microhematuria and proteinuria. His next visit to a medical institution was in 2002 at 38 years of age and revealed urine protein 2+, urine occult blood 1+, plasma Cr 1.13 mg/dl and hypertension. An angiotensin receptor blocker (ARB) was started. After that, he saw a doctor regularly, but hematuria and proteinuria became gradually worse. A relapse of IgA nephropathy was suspected. In March 2009, he was admitted to a hospital for renal biopsy to evaluate the progression of IgA nephropathy.
The patient's general condition at the time of hospitalization was height 163.0 cm, weight 55.0 kg, body mass index 20.7 kg/m2, blood pressure 116/72 mmHg, heart rate 83 beats/min and temperature 36.6 °C. He was lucid with no sign of anemia in the palpebral conjunctiva. No swelling of the throat, abnormal chest auscultation, hard and tender points in the abdominal area or edema of the extremities was observed. Medical examinations (Table ) revealed urine protein 3+ (0.90 g/day), urine occult blood 3+ (RBC 10–19/HPF) and serum Cr 1.63 mg/dl.
Renal biopsy (Fig. ) showed 4 global scleroses, 3 cellular crescent formations and 3 adhesions in 28 glomeruli; moderate expansion of the mesangial matrix; moderate tubular atrophy with mild cell infiltration in the interstitium; and moderate arteriolosclerosis and thickening of interlobular arteries. Immunostaining of IgA confirmed the diagnosis of active chronic-progressive IgA nephropathy.
After admission, the patient was treated with tonsillectomy and steroid pulse therapy. Steroid pulse therapy was given as follows: methylprednisolone was administered continuously at a pulsed dose of 500 mg/day for 3 days, followed by oral prednisolone at a dose of 30 mg continuously for 3 weeks. After completion of the third course, oral prednisolone was initiated at a dose of 30 mg/day every other day after treatment and tapered by 5 mg every 2 months. The after-treatment follow-up was continued for 1 year. The patient underwent tonsillectomy after discharge from the hospital (day 75) and was then followed up at the outpatient clinic. He completed oral prednisolone treatment in approximately a year, but continued taking an ARB during the follow-up period. Clinical remission was achieved 7 months after the initiation of therapy (Table ), and hematuria and proteinuria were no longer observed in this 3-year follow-up period (Fig. ). | 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. | 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 1.63 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 163.0 cm, which is 163.0 cm * 1 m / 100 cm = 1.63 m. The patient's weight is 55.0 kg. The patient's bmi is therefore 55.0 kg / (1.63 m * 1.63 m) = 20.701 kg/m^2.The patient's BMI is 20.7, 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 - 43) * 55.0 * 1) / (1.63 * 72) = 45.458 mL/min. Hence, the patient's creatinine clearance is 45.458 mL/min. | 45.458 |
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} | medical_problem | A 45-year-old woman comes to the physician because of fatigue and irregular menstrual cycles for the past year. She also complains of recurrent sinus infections. During the past 6 months, she has had increased urinary frequency and swelling of her feet. She has also had difficulty lifting her 3-year-old niece for the past 3 weeks. She was recently diagnosed with depression. She works as a medical assistant. The patient has smoked one half-pack of cigarettes daily for 25 years and drinks four beers on the weekends. Her only medication is escitalopram. She is 160 cm (5 ft 3 in) tall and weighs 79 kg (175 lb); BMI is 31 kg/m2. She appears tired. Her temperature is 37°C (98.6°F), pulse is 80/min, respirations are 18/min, and blood pressure is 140/82 mm Hg. Physical examinations shows neck obesity and an enlarged abdomen. Examination of the skin shows multiple bruises on her arms and legs. There is generalized weakness and atrophy of the proximal muscles. Laboratory studies show:
Serum
Na+ 150 mEq/L
K+ 3.0 mEq/L
Cl- 103 mEq/L
HCO3- 30 mEq/L
Urea nitrogen 19 mg/dL
Creatinine 0.9 mg/dL
Glucose 136 mg/dL
A 1 mg overnight dexamethasone suppression test shows a serum cortisol of 167 nmol/L (N < 50) and a 24-hour urinary cortisol is 425 μg (N < 300 μg). Serum ACTH is 169 pg/mL (N = 7–50). Subsequently, a high-dose dexamethasone suppression test shows a serum cortisol level of 164 nmol/L (N < 50). | 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. | 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 45 years old.
The concentration of creatinine is 0.9 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 160.0 cm, which is 160.0 cm * 1 m / 100 cm = 1.6 m. The patient's weight is 79.0 kg. The patient's bmi is therefore 79.0 kg / (1.6 m * 1.6 m) = 30.859 kg/m^2.The patient's BMI is 30.9, 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 160.0 cm, which is 160.0 cm * 0.393701 in/cm = 62.992 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 * (62.992 (in inches) - 60) = 52.382 kg.
Hence, the patient's IBW is 52.382 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 = 52.382 kg + 0.4 * (79.0 kg - 52.382 kg) = 63.029 kg. The patient's adjusted body weight is 63.029 kg.
Using the Cockcroft-Gault equation:
CrCl = ((140 - age) * adjusted weight * gender_coefficient) / (serum creatinine * 72).
Plugging the patient's values gives us ((140 - 45) * 63.029 * 0.85) / (0.9 * 72) = 78.543 mL/min. Hence, the patient's creatinine clearance is 78.543 mL/min. | 78.543 |
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} | medical_problem | A 57-year-old-male patient 165 cm tall, and weighing 68 kg in the ASA 1 risk group because of numbness of his left wrist. The biochemical parameters of the patient who was scheduled for operation under regional anesthesia with the diagnosis of carpal tunnel syndrome were as follows; Hb:14.0 mg/dL, Htc:43.0%, Plt:229000/mm3, WBC:6000/mm3, FBG:100 mg/dL, BUN:2817 mg/dL, Creatinine:0.7 mg/dL, AST:20.72 mg/dL, and ALT:12.45 mg/dL. His electrocardiogram (EKC) revealed a HR of 70 bpm with normal sinus rhythm.
Preoperatively the patient was informed about axillary nerve blockade, and his written informed consent was obtained. He didn’t receive any preoperative premedication, and in the operating room, his standard EKG, peripheral O2 saturation (SpO2), and noninvasive blood pressure (NIBP) were monitores. Using a 18 G branule a vein on the back of his left hand was punctured, and 0.09%NaCl infusion at a rate of 200 ml/hr was initiated. Right arm to be operated was positioned at 90° abduction with the torso, and forearm was flexed 90°. After cleansing the surgical field with a sterile antibacterial solution, the site was covered with sterile drape, and a single injection was made with a 22 G x 50 mm needle (Stimuplex® Braun, Melsungen, Germany). Retrograde blood was not observed during negative aspiration.
Using a peripheral nerve stimulator (Stimuplex A; B.Braun Melsungen AG, B.Braun Medical AG CH-6021, Germany) at an intensity of 1.5 mA the nerve was localized. When the intensity of the electrical current was reduced to 0.5 mA, nervous stimuli were observed which made us to think that we were on the innervation site of the nerve to be blocked. Then 40 mL anesthetic solution preprepared by anesthesia technician which we thought to be our routinely used mixture i.e. [20 mL 1% lidocaine (2 ampoules of 2% lidocaine, and 10 mL NaCl 0.09%) and 20 mL 1% prilocaine (10 mL 2% prilocaine, and 10 mL0,09% NaCl)] was injected to the patient with negative suctions after each application of 5 mL. Injection site was compressed for 5 minutes. Nearly 10 minutes later the patient felt numbness on his tongue, irritability, restlessness, agitation, he uttered meaningless words, and moved his arms, and legs senselessly. Decreased peripheral oxygen saturation and presence of peripheral cyanosis led us to make an initial diagnosis of methemoglobinemia, and supportive O2 therapy was initiated via oxygen mask at a rate of 6 lt per minute. We couldn’t measure methemoglobin levels because of lack of necessity facilities. Arterial blood gas measurements were as follows. pH: 7.43 pO2:60.1, and pCO2:44.0. Respiratory distress of the patient increased, and deepened, with a drop in his SpO2 to 76, was intubated under 1 mg/kg propofol, 1 µ/kg fentanyl, and 0.5 mg.kg−1 rocuronium anesthesia to enjure the patency of his airway. For the post-intubation maitenance of anesthesia 50 oxygen –nitrogen, and 1 mac sevoflurane were used. Following induction of anesthesia, hypotension (NIBP: 60/40 mmHg), and bradycardia (HR:40 bpm) developed which required administration of 0.5 mg atropin, and intermittent IV injections of ephedrine (total dose 30 mg). When his health state was stabilized, NIBP values improved, and his HR dropped to 70 bpm with SpO2: 95%, he was amenable for surgery. At the end of the operation which lasted for nearly half an hour, the patient was awakened with injections of 10 µg/kg atropine, and 40 µg/kg neostigmine. Thoughy the patient still continued to articulate meaningless words, and make senseless movements, since he was more cooperative we transferred the patient into the intensive care unit.
When we discerned that in place of 2% lidocaine ampoule which we always requested as a local anesthetic from the pharmacy, 10% lidocaine ampoule was sent, and anesthetic mixture was prepared without checking whether it was 2% lidocaine, we made the diagnosis of local anesthetic intoxication related to wrong formulation of lidocaine rather than methemoglobinemia
During 24-hour monitorization in the intensive care unit his hemodynamic parameters were stable, and his complaints resolved. Then the patient was traansferred to his service with relevant recommendations. | 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. | 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 57 years old.
The concentration of creatinine is 0.7 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 165.0 cm, which is 165.0 cm * 1 m / 100 cm = 1.65 m. The patient's weight is 68.0 kg. The patient's bmi is therefore 68.0 kg / (1.65 m * 1.65 m) = 24.977 kg/m^2.The patient's BMI is 25.0, 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 Male.
The patient's height is 165.0 cm, which is 165.0 cm * 0.393701 in/cm = 64.961 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 * (64.961 (in inches) - 60) = 61.41 kg.
Hence, the patient's IBW is 61.41 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 = 61.41 kg + 0.4 * (68.0 kg - 61.41 kg) = 64.046 kg. The patient's adjusted body weight is 64.046 kg.
Using the Cockcroft-Gault equation:
CrCl = ((140 - age) * adjusted weight * gender_coefficient) / (serum creatinine * 72).
Plugging the patient's values gives us ((140 - 57) * 64.046 * 1) / (0.7 * 72) = 105.473 mL/min. Hence, the patient's creatinine clearance is 105.473 mL/min. | 105.473 |
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} | medical_problem | A 51-year-old gentleman, recently diagnosed to have type 2 diabetes mellitus and systemic hypertension, presented to the cardiology outpatient clinic on 28th July 2016 with history of pricking chest pain and shortness of breath for the past 7 years and recurrent attacks of syncope since the previous year. He weighed 49 kg and with a height of 157 cm; body mass index was 19.88 kg/m2. His blood pressure (BP) was 120/80 mmHg and pulse rate was 78/min and regular in rhythm. He was afebrile. Systemic examination was unremarkable.
Laboratory findings revealed hemoglobin of 15.1 g/dL, hematocrit of 47%, white blood cell count of 11,300/mm3 (differential count of neutrophils of 56%, lymphocytes 26%, eosinophils 11%, and monocytes of 7%), and platelet count of 293,000/mm3. Urine on routine examination showed a pH of 6.0, specific gravity of 1015, and was negative for albumin, glucose, red blood cells, and pus cells. Blood glucose fasting was 115 mg/dL and post-prandial was 219 mg/dL with an HbA1C of 7.1%. Blood urea was 27 mg/dL and creatinine was 1.0 mg/dL. Serum electrolytes were as follows: sodium 141 mEq/L, potassium 4.3 mEq/L, chloride 103 mEq/L, and bicarbonate 28 mEq/L. Serum cholesterol was 183 mg/dL, serum triglyceride 121 mg/dL, and serum uric acid 3.9 mg/dl. Two-dimensional (2D) echocardiogram showed normal left ventricular dimensions, no regional wall motion abnormality, and a left ventricular ejection fraction of 69%. Holter monitoring showed occasional supraventricular and ventricular premature complexes. On 2nd August, coronary angiography showed insignificant coronary artery disease with dominant right coronary system and he was discharged with medical advice.
On 3rd August, he attended emergency department with complaints of severe back pain, palpitation, and sweating. His back pain was sudden in onset, gradually progressive, throbbing type, rating 8/10 in pain scale, radiating to the left flank, aggravated by exertion, and partially relieved by rest. He had no other complaints. He was on metformin and calcium channel blocker. He looked anxious, agitated, and restless but was oriented and afebrile. His pulse rate was 112/min, respiratory rate was 28/min, and BP was 210/120 mmHg in the right upper limb and 210/100 mmHg over the left upper limb in supine position. There was no radio-femoral delay. Systemic examination was unremarkable except for a mild tenderness in the lumbar region.
On investigation, electrocardiography, chest X-ray, complete blood counts, liver function tests, 2D echocardiography, urine analysis, and toxicology screen were all within normal limits. Serum amylase and lipase were normal. Blood urea was 58 mg/dL and serum creatinine was 2 mg/dL. Venous blood gas (VBG) analysis showed a pH of 7.21, bicarbonate of 18 mmol/L, base excess of −9.4 mmol/L, and a lactate of 10.81 mmol/L. Serum electrolytes were sodium 138 mmol/L, potassium 3.8 mmol/L, and chloride 108 mmol/L, and anion gap was 12 mmol/L.
The following were considered in the differential diagnosis of this situation: (a) acute mesentric ischemia, (b) aortic dissection (c) hypertensive emergency, and (d) pancreatitis. Contrast-enhanced computed tomography abdomen showed a lesion in the left adrenal gland measuring about 3.5 × 3.2 cm with mild enhancement in the arterial phase, features consistent with pheochromocytoma [: Contrast enhanced CT scan of abdomen showing the mildly enhancing left adrenal mass]. No additional extra-adrenal tumors were seen. There was no evidence of mesenteric ischemia, aortic dissection, or pancreatitis. Upon further questioning his family members, it was known that he was unwell in the previous 6 months with on and off headache, palpitation, and anxiousness, which they attributed to the recently diagnosed diabetes mellitus.
His BP was managed with alpha adreno-receptor blocker and calcium channel blocker. Phenoxybenzamine was added at a dose of 10 mg twice a day and later increased to 20 mg three times daily. Persistent tachycardia and BP were stabilized with addition of beta blocker.
On 5th August 2016, the level of 24-h urine metanephrines was 14,536 mcg (reference range: less than 350 mcg/24 h) and nor-metanephrines was 7,607 mcg (reference range: less than 600 mcg/24 h).
Laparoscopic removal of pheochromocytoma was done under general anesthesia on 12th August 2016. After the surgery, there was a brief episode of hypoglycemia and hypotension, which was managed with 25% dextrose and normal saline, respectively. Azotemia resolved and blood gases were normalized. Pathological examination of the resected mass revealed a well-encapsulated tumor of size 5 cm × 4 cm × 3 cm, without hemorrhage. It showed polygonal and round cells with abundant cytoplasm and increased vasculature. There was no capsular or vascular invasion. Tumor cells were seen in the background of spindle cells with ganglion cells and Schwanian stroma. These features were reported as consistent with a CP–ganglioneuroma of the left adrenal gland []. Immunohistochemistry examination showed positivity for chromogranin, synaptophysin, and S-100 stains and negativity for calretinin in pheochromocytoma cells. Calretinin, chromogranin, synaptophysin, and S-100 stains were positive in the ganglioneuromatous component. Vimentin was positive and cytokeratin was negative. These staining characteristics confirmed the composite nature of the tumor.
At the time of discharge, his blood pressure and blood glucose were normal. Upon review on 28th February 2017, his BP was 130/80 mmHg without antihypertensive medicine. Blood glucose fasting was 90 mg/dL and post-prandial 66 mg/dL, with an HbA1C of 6.1% without any antidiabetic medicine. The levels of 24-h urinary metanephrines and normetanephrines were 62 and 604, mcg, respectively. | 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. | 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 51 years old.
The concentration of creatinine is 2.0 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 157.0 cm, which is 157.0 cm * 1 m / 100 cm = 1.57 m. The patient's weight is 49.0 kg. The patient's bmi is therefore 49.0 kg / (1.57 m * 1.57 m) = 19.879 kg/m^2.The patient's BMI is 19.9, 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 49.0 kg.
Using the Cockcroft-Gault equation:
CrCl = ((140 - age) * adjusted weight * gender_coefficient) / (serum creatinine * 72).
Plugging the patient's values gives us ((140 - 51) * 49.0 * 1) / (2.0 * 72) = 30.285 mL/min. Hence, the patient's creatinine clearance is 30.285 mL/min. | 30.285 |
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} | medical_problem | A 12-year-old boy, average student of class VII, presented with 1 year history of generalized tonic clinic seizures which lasted for 2-3 min. In the initial 2-3 days of his illness, he had 2-3 seizures daily for which he received carbamazepine 200 mg twice daily. Seizure though was controlled, but he started having carpopedal spasms lasting for 1-2 min. His elder brother aged 16 years also had similar illness. Examination revealed that the patient was of average built and nutrition (height 157.5 cm, weight 48kg) and there were no dysmorphic features. The neurological examination was normal except Trousseau’s sign.
The laboratory studies revealed normal hemoglobin and blood counts. His serum calcium was 6 (ionized 4) (normal 8.5-10.8, ionic 4.6-5.3) mg/dl, phosphorus 8 (normal 2.5-4.5) mg/dl, alkaline phosphatase 999 U/l, and magnesium 2.2 mg/dl, blood urea nitrogen 8 mg/dl, and creatinine 0.7 mg/dl. 24-h urinary calcium was 150 (normal 200) mg, phosphorous 0.06 (normal 1) g, and creatinine 1.29 (normal 1-2) g. His calculated TmP/GFR was 2.57 mmol/l (normal 1.15-2.44 mmol/l for 2-15 years age).[] The glomerular filtration rate was 122 ml/min. Serum 25-OH vitamin D was 9.98 (normal 9-47) ng/ml and PTH 335.4 (normal 9-55) pg/ml. His electrocardiogram, electroencephalography, radiograph of hand, feet and pelvis were normal. CT scan revealed bilateral hyperdensity in bilateral caudate, globus pallidus, putamen, and right frontal white matter. Cranial MRI revealed T1 hyperintensity in caudate, globus pallidus, putamen, and dentate nuclei bilaterally. T2 and FLAIR images were normal. He was prescribed calcitrol 0.25 mg twice daily and calcium gluconate 500 mg four times daily without anticonvulsant, on which he was asymptomatic till 1 year follow up. | 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. | 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 12 years old.
The concentration of creatinine is 0.7 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 157.5 cm, which is 157.5 cm * 1 m / 100 cm = 1.575 m. The patient's weight is 48.0 kg. The patient's bmi is therefore 48.0 kg / (1.575 m * 1.575 m) = 19.35 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 48.0 kg.
Using the Cockcroft-Gault equation:
CrCl = ((140 - age) * adjusted weight * gender_coefficient) / (serum creatinine * 72).
Plugging the patient's values gives us ((140 - 12) * 48.0 * 1) / (0.7 * 72) = 121.905 mL/min. Hence, the patient's creatinine clearance is 121.905 mL/min. | 121.905 |
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"Row Number": 29,
"Upper Limit": "100.576"
} | medical_problem | A 26-year-old man with progressive chest pain and respiratory distress was transported
as an emergency case to our hospital from the local airport. He had just returned to
Japan from traveling in southeastern Asia for 1 week. He had no relevant past medical
history and was not on medication. He had developed pain in the right lower mandibular
area over the past week. The pain had progressed from the neck to the chest; he
developed a high fever during his journey and could not eat or drink. In the emergency
room, peripheral oxygen saturation was 95% with receiving oxygen at 15 L/min via an
oxygen mask and a reservoir bag. A chest X-ray showed a slightly widened mediastinum
with pleural effusion (). An
ECG revealed widespread ST-elevation (). Physical examination revealed a body mass index of 23.0 kg/m2
(height 168.0 cm; weight 65.0 kg), blood pressure of 121/68 mmHg, average heart rate of
110/min, respiratory rate of 40 breaths/min, body temperature of 37.9°C, and
tenderness and redness in the anterior and bilateral sides of the neck. White blood cell
count was 14,510/µL, neutrophils were 11,320/µL, red blood cell count
was 5.07×106/µL, hemoglobin was 14.7 g/dL, and the platelet
count was 196,000/µL. C-reactive protein level was elevated at 54.52 mg/dL (ref.
0.0–0.14 mg/dL). Blood urea nitrogen and creatinine levels were 45 mg/dL (ref.
8–20 mg/dL) and 1.06 mg/dL (ref. 0.65–1.07 mg/dL), respectively. Lactate
dehydrogenase was elevated to 510 U/L (ref. 124–222 U/L). Creatine kinase and
creatine kinase-MB were 269 (ref. 59–248 U/L) and 11.6 (ref. 0.0–12.0
U/L), respectively. The fasting blood glucose and HbA1c levels were normal. Although
these findings indicated the possibility of acute pericarditis, an ECG did not show any
findings of pericarditis or myocardial dysfunction. Contrast-enhanced CT images revealed
that a large volume of gas had collected in the neck and upper and anterior mediastinum
(). In addition,
an abscess had formed in the retropharyngeal, bilateral sub-mandibular, upper
paratracheal, and mediastinal spaces with pleural effusion and atelectasis in the right
lower basal lobe (). Thus, DNM induced by odontogenic infection with a right mandibular
second or third molar abscess was highly suspected.
A multidisciplinary team, including physicians, otolaryngologists, surgeons, and
intensivists commenced treatment within 2 hours of arrival. He received intravenous 600
mg clindamycin bid and 4.5 g tazobactam/piperacil-lin hydrate qid. A tracheostomy,
bilateral neck drainage, neck fasciotomy, and debridement via a cervical incision were
performed 5 hours after arrival. The blood culture on admission was negative.
Gram-positive cocci were found in sputum and pus, and Streptococcus
pyogenes, Streptococcus constellatus, Fusobacterium
necrophorum, and Peptostreptococcus sp. were found later in
pus culture. Continuous bilateral thoracic drainage began due to the development of a
bilateral pyothorax. Subsequently, the transcervical mediastinal and right mediastinal
areas were drained via thoracotomy. His condition improved steadily, and he was
discharged without any comorbidities on hospital day 63 after admission. Pathological
findings from the excised skeletal muscle and fascia indicated acute inflammation with
necrosis (),
consistent with necrotizing fasciitis, and a large number of Gram-positive cocci were
observed (). Thus, the
radiological diagnosis of DNM was confirmed histologically and bacteriologically. | 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. | 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 26 years old.
The concentration of creatinine is 1.06 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 168.0 cm, which is 168.0 cm * 1 m / 100 cm = 1.68 m. The patient's weight is 65.0 kg. The patient's bmi is therefore 65.0 kg / (1.68 m * 1.68 m) = 23.03 kg/m^2.The patient's BMI is 23.0, 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 64.127 kg.
Using the Cockcroft-Gault equation:
CrCl = ((140 - age) * adjusted weight * gender_coefficient) / (serum creatinine * 72).
Plugging the patient's values gives us ((140 - 26) * 64.127 * 1) / (1.06 * 72) = 95.787 mL/min. Hence, the patient's creatinine clearance is 95.787 mL/min. | 95.787 |
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"Row Number": 30,
"Upper Limit": "35.75"
} | medical_problem | A 66-year-old man (body height, 168 cm; body weight, 88.5 kg) experienced dyspnea, a sensation of chest tightness, and back pain for a few days before he was brought to our hospital on an emergency basis. His symptoms became aggravated suddenly as he was about to get off a taxi on his way home from work. He presented with a history of close contact with a coworker with COVID-19 and was waiting for instructions from a public health center.
In the ambulance, the following conditions were documented: Glasgow Coma Scale score, E4V5M6; heart rate, 80/min and irregular; blood pressure, 100/60 mmHg; body temperature, 38.4ºC; oxygen saturation, 98% (O2 delivered with reservoir mask at a rate of 15 L/min). On admission, his white blood cell count was 22,300/µL; hemoglobin, 14.7 g/dL; platelet count, 35 × 104/µL; creatinine level, 2.23 mg/dL; creatine kinase level, 2582 IU/L; creatine kinase myocardial band level, 164 ng/mL; low-density lipoprotein cholesterol level, 97 mg/dL; high-density-lipoprotein cholesterol level, 19 mg/dL; triglyceride level, 173 mg/dL; hemoglobin A1c level, 7.9%; C-reactive protein level, 13.8 mg/dL; troponin T level, 9.640 ng/mL; N-terminal pro-brain natriuretic peptide level, 11753 pg/mL; procalcitonin level, 0.62 ng/mL; d-dimer level, 16.34 µg/mL; and soluble fibrin level, 113.1 µg/mL. An electrocardiogram showed atrial fibrillation; ST-elevation in II, III, aVF, and V2–V6 leads; and ST depression in aVR leads (Figure ). Echocardiography revealed severe hypokinesis extending from the anterior wall to the apex and the inferior wall in left ventricle, with an approximate ejection fraction of 20%. We diagnosed STEMI and decided to perform emergency coronary angiography (CAG). A chest radiograph showed infiltrative shadows in both lungs and tracheal intubation was performed in the emergency outpatient unit (Figure ). Continuous infusion of noradrenaline (0.1 μg/kg/min) was started because his systolic blood pressure dropped below 80 mmHg. After heparin (5,000 U) was administered intravenously, the patient was transferred to the cardiac catheterization room.
CAG was performed by cardiologists, emergency physicians, clinical engineers, nurses, and radiological technologists who donned appropriate personal protective equipment before entering the room. CAG revealed total occlusion of the middle of the right coronary artery (RCA) and left anterior descending artery (LAD; Figure ). After a loading dose of dual antiplatelet therapy (aspirin, 162 mg; clopidogrel, 300 mg), an intra-aortic balloon pump catheter was inserted, and a 7-Fr guiding catheter was inserted into the left coronary artery. We removed white material, which did not at a first glance appear to be a typical thrombus, with an aspiration catheter, but blood flow did not improve. The onset-to-device time and door-to-device time were 116 and 84 minutes, respectively. Subsequent intravascular ultrasonography (IVUS) revealed several structures, which were thought to be thrombi; therefore, we performed plain old balloon angioplasty (Figure ). After the balloon was expanded, blood flow improved slightly in the LAD but not distally. Next, we placed an everolimus-eluting stent (4.0 × 38 mm) in the middle of the LAD, but peripheral blood flow was still not observed. Repeated IVUS revealed severe stenosis caused by plaque with thrombi. An additional balloon was inflated at the distal site, and a cutting balloon was also used. Another everolimus-eluting stent (2.25 × 38 mm) was placed at the distal site, but no blood flow improvements were seen angiographically.
We moved a double-lumen catheter to the distal LAD and performed CAG from the distal LAD, which revealed retrograde blood flow up to the middle of the LAD and collateral circulation from the septal branch to the RCA. Repeated IVUS examination revealed thrombi and plaque at the distal end of the stent and no intrastent blood flow (Figure ). Then, we tried to perform PCI for the total occlusion of RCA, but it was unsuccessful. At this point, 7 hours passed since the patient entered the cardiac catheterization room, and so we finished the procedure. The levels of activated clotting time during PCI were maintained at 280–310 seconds. After PCI, pathological examination proved the aspirated white material was white thrombi. Chest computed tomography performed after PCI showed ground-glass opacities distributed unevenly in both the lungs, as well as left-sided pleural effusion (Figure ). After the patient was transferred to the intensive care unit, he showed pulseless electrical activity, and cardiopulmonary resuscitation (CPR) was initiated. Return of spontaneous circulation was achieved with 1 mg of epinephrine and one cycle of CPR. Veno-arterial extracorporeal membrane oxygenation was considered, but his family decided against it. The blood pressure was maintained through the continuous administration of noradrenaline, dobutamine, and adrenaline. His nasopharyngeal swab was tested with polymerase chain reaction for SARS-CoV-2, and COVID-19-related pneumonia was diagnosed. Remdesivir treatment was initiated at a dose of 200 mg/day on the 5th day of hospitalization and continued at 100 mg/day. Because of the possibility of concomitant bacterial pneumonia, ampicillin sodium/sulbactam sodium (9 g/day) was also administered. However, the patient's oxygenation level worsened, and he died on the 7th day. It was difficult to confirm a main cause of death because we were not permitted to dissect patients due to COVID-19. We assumed that he had died from both cardiogenic shock due to myocardial infarction and septic shock due to covid-19 infection. | 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. | 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 66 years old.
The concentration of creatinine is 2.23 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 168.0 cm, which is 168.0 cm * 1 m / 100 cm = 1.68 m. The patient's weight is 88.5 kg. The patient's bmi is therefore 88.5 kg / (1.68 m * 1.68 m) = 31.356 kg/m^2.The patient's BMI is 31.4, 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 168.0 cm, which is 168.0 cm * 0.393701 in/cm = 66.142 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 * (66.142 (in inches) - 60) = 64.127 kg.
Hence, the patient's IBW is 64.127 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 = 64.127 kg + 0.4 * (88.5 kg - 64.127 kg) = 73.876 kg. The patient's adjusted body weight is 73.876 kg.
Using the Cockcroft-Gault equation:
CrCl = ((140 - age) * adjusted weight * gender_coefficient) / (serum creatinine * 72).
Plugging the patient's values gives us ((140 - 66) * 73.876 * 1) / (2.23 * 72) = 34.048 mL/min. Hence, the patient's creatinine clearance is 34.048 mL/min. | 34.048 |
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"Row Number": 31,
"Upper Limit": "150.51"
} | medical_problem | A 26-year-old man arrived at the emergency department with a seven-day history of hematemesis and melena. He had no previous medical history and did not drink alcohol or used any illicit drug or medication.
Physical examination on admission showed blood pressure of 100/60 mmHg, a temperature of 36°C (96.8°F), a pulse rate of 90/min, and a respiratory rate of 22/min; his height was 1.75 m, weight 98 kg, and BMI 32 kg/m2. He experienced pain with deep palpation in the epigastrium and no organomegaly or lymphadenopathy was identified. The left scrotal sac was enlarged and indurated and there was a mass in the left scrotum that was indistinguishable from the left testis and provoked displacement of structures of the penis and right testis (the right scrotum was empty). No inguinal lymphadenopathy was identified.
Laboratory tests revealed normal liver function. Hemoglobin was 9.13 g/dl, MCV was 87.9 fL, WBC was 11.9 K/uL, neutrophils were 9.81 K/uL, lymphocyte count was 1.59 K/uL, and platelet level was 252 K/uL. Serum glucose level was 106 mg/dl, BUN was 38 mg/dl, creatinine was 0.9 mg/dl, and calcium was 8.9 mg/dl. Serum alpha-fetoprotein (AFP) level was 17,090 ng/mL, lactate dehydrogenase was 1480 U/L (normal range: 91–180 IU/L), and human chorionic gonadotropin level was 287.4 IU/mL.
After resuscitation with crystalloid solutions, he underwent upper endoscopy. The gastroenterologist found abundant active bleeding, for which orotracheal intubation was decided to provide airway protection. The patient was transferred to the intensive care unit. A second upper endoscopy revealed a type 1 isolated gastric varix, treated with cyanoacrylate without complications ().
A scrotal US showed a large heterogeneous image in the left testicle area, with an echogenic and cystic solid component and flow presence with color Doppler assessment.
A contrasted CT scan of the thorax, abdomen, and pelvis showed a liver of normal size and density with multiple retrocrural, retroperitoneal, mesenteric, and left iliac metastatic lymphadenopathy which caused extrinsic compression of the portal vein along with splenic vein partial thrombosis with left-sided portal hypertension and perigastric and perisplenic collateral neovascularization (). A heterogeneous, well defined mass was found in the left testicle, 16.7 × 16.1 × 14.9 cm, with a solid component that was enhanced with the administration of contrast, as well as a cystic component. There was also invasion of the left spermatic cord.
The patient was extubated after surveillance and transferred to the Internal Medicine Department. We started chemotherapy with etoposide 100 mg/m2 and cisplatin 20 mg/m2, and seven days later the patient underwent a left radical orchiectomy by an inguinal approach with left hemiscrotectomy, without complications. Following this intervention, serum alpha-fetoprotein (AFP) level was reduced to 350 ng/mL, and the human chorionic gonadotropin level was 50 IU/mL.
A postoperative biopsy showed a pure testicular teratoma () with glandular formations and the presence of cartilage (a) and respiratory epithelium, with ciliated columnar cells alternating with goblet cells (b).
The patient was discharged after showing clinical improvement to receive ambulatory chemotherapy. | 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. | 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 26 years old.
The concentration of creatinine is 0.9 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 1.75 m. The patient's weight is 98.0 kg. The patient's bmi is therefore 98.0 kg / (1.75 m * 1.75 m) = 32.0 kg/m^2.The patient's BMI is 32.0, 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 Male.
The patient's height is 1.75 m, which is 1.75 m * 39.3701 in/m = 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 * (98.0 kg - 70.465 kg) = 81.479 kg. The patient's adjusted body weight is 81.479 kg.
Using the Cockcroft-Gault equation:
CrCl = ((140 - age) * adjusted weight * gender_coefficient) / (serum creatinine * 72).
Plugging the patient's values gives us ((140 - 26) * 81.479 * 1) / (0.9 * 72) = 143.343 mL/min. Hence, the patient's creatinine clearance is 143.343 mL/min. | 143.343 |
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} | medical_problem | A 21-year-old Japanese woman was admitted to our hospital because of proteinuria and hematuria. She had been diagnosed at birth with persistent cloaca and congenital esophageal atresia, and underwent enterostomy, cystostomy, and radical esophageal surgery, followed by repair of persistent cloaca and colostomy closure 2 years later. She was followed-up at the pediatric surgery and urology department, and developed with no major problems. Proteinuria and hematuria were detected at routine examination 7 months prior to admission for the first time. No urological problems were detected at a visit to the urology department 3 months before admission. She had mild edema before admission; however its onset had been gradual and it was therefore not clear when the edema had started.
On admission, the patient’s height was 158.6 cm, her weight was 53.0 kg, and her blood pressure was 101/80 mmHg. Physical examination revealed an abdominal midline operation scar and pretibial pitting edema. Urinary examination revealed a protein level of 3+ and 5–9 red blood cells per high-power field. Her urine protein/creatinine ratio was 3.38 g/gCr, blood urea nitrogen was 13.2 mg/dL, serum creatinine was 0.73 mg/dL, and serum albumin was 3.6 g/dL. Serum C3 was 25 mg/dL, C4 was 18.5 mg/dL, and 50% hemolytic unit of complement (CH50) was 13 U/mL. Chromosome G banding revealed a normal karyotype 46XX. Kidney ultrasound showed no kidney deformity. Kidneys size was normal.
A renal biopsy contained 24 glomeruli, all of which showed moderate to severe mesangial hypercellularity and increased homogenous materials in the mesangium. Which were positive with periodic acid-Schiff and were negative with methenamine silver (Fig. ). One glomerulus revealed fibrous crescent formation, and 11 showed segmental double contour of glomerular basement membrane. Immunofluorescence microscopy showed slight staining for fibrinogen, but no staining for IgG, IgA, IgM, kappa light chain and lambda light chain (Fig. ). Electron microscopy showed massive granular deposits in the mesangial area and some subepithelial area (Fig. ). According to these findings, we speculated fibronectin glomerulopathy as a diagnosis. Thus, we performed immunoassays using anti-human fibronectin antibodies. The staining with IST-4, which detects plasma and cell-associated fibronectin, was positive but no staining was observed with IST-9, which stains only cell-associated fibronectin (Fig. ). The mesangial deposits were therefore shown to comprise plasma fibronectin. The patient was finally diagnosed as fibronectin glomerulopathy.
Her family history was investigated further. Although her mother and younger sister had previously been detected to have proteinuria, their urine and blood tests were normal. Her father showed no urinary abnormalities and normal kidney function at his annual health examination. Given that no family history of renal disease could be identified, the current case was determined to be sporadic. The patient and her mother underwent genetic testing of the FN1 gene, which revealed no abnormalities.
Treatment with an angiotensin II receptor antagonist and a sodium-restricted diet were started. However, 10 months after the kidney biopsy, the patient’s proteinuria had increased and her renal function was deteriorated, with a urine protein/creatinine ratio of 9.52 g/gCr, serum creatinine 0.86 mg/dL. Her serum albumin decreased to 2.0 g/dL. | 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. | 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 21 years old.
The concentration of creatinine is 0.73 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 158.6 cm, which is 158.6 cm * 1 m / 100 cm = 1.586 m. The patient's weight is 53.0 kg. The patient's bmi is therefore 53.0 kg / (1.586 m * 1.586 m) = 21.07 kg/m^2.The patient's BMI is 21.1, 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 51.114 kg.
Using the Cockcroft-Gault equation:
CrCl = ((140 - age) * adjusted weight * gender_coefficient) / (serum creatinine * 72).
Plugging the patient's values gives us ((140 - 21) * 51.114 * 0.85) / (0.73 * 72) = 98.367 mL/min. Hence, the patient's creatinine clearance is 98.367 mL/min. | 98.367 |
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"Upper Limit": "24.75"
} | medical_problem | A 41-year-old male was referred to our Nephrology Unit because of worsening of kidney function and proteinuria. He was born at term of a normal pregnancy from apparently healthy, nonconsanguineous parents. The patient's early development was normal and he had no evident clinical problem until 18 years of age, when he developed seizures triggered by light and recurrent headaches. He was prescribed Valproic Acid and started a discontinuous follow-up in Neurology. In 1991 (age 22) EEG revealed well-represented alpha background activity, with a complex wave-peak after 7-10 flashes/sec, an expression of an epileptogenic photosensitive centroencephalic focus. In 1992, in the presence of signs of myopathy (asthenia, increase of serum lactate, myalgia), a muscle biopsy showed non-specific changes (occasional small red sub-sarcolemmal deposits, showing oxidative enzymatic activity). In 1992 the patient's sister (3 years younger) developed generalized seizures and myopathy. Genetic counseling suggested the presence of a mitochondrial disease.
Detection of the 3243A > G mutation of mitochondrial DNA confirmed the diagnosis of MELAS syndrome in the patient, his sister, his mother and one of the mother's sisters.
In the subsequent decade, he started and discontinued different types of anticonvulsant therapy (including Lamotrigine and Phenobarbital), and developed recurrent seizures, with imaging evidence of an ischemic lesion in the left hemisphere, progressive bilateral sensorineural hearing loss and sensitive distal polyneuropathy with increasing muscle weakness. On various occasions, lactic acidosis was found (lactic acid 10-13.5 mmol/L; normal <2 mmol/L).
In July 2009 (age 39) he was diagnosed with diabetes mellitus (weight loss, polyuria and polydipsia); at diagnosis, glycated hemoglobin was 19.6% and glycemia <500 mg/dL. Insulin treatment was started. Soon after diagnosis, he developed a sepsis due to Klebsiella pneumoniae. A CT scan, performed on the suspicion of a pyelonephritis focus, showed a solid hypervascularized mass, highly suggestive of neoplasia, in the right kidney. During hospitalization, serum creatinine was 0.9 mg/dL; 24-hour proteinuria was absent at repeated urinalysis; glomerular filtration rate (eGFR) was 62 mL/min (Cockcroft and Gault formula). He was normotensive (usual blood pressure 120/80 mmHg) and remained so during follow-up.
In November 2009 the patient underwent right nephrectomy. At surgery, a second small superficial tumor was detected. The histological examination identified a renal oncocytoma (2 cm); a smaller lesion (0.5 cm) had an appearance highly suggestive of chromophobe carcinoma. However, the lesion could also represent a tumoral focus of tubular oncocytosis and a precursor of another oncocytoma (Figures and ). The cytogenetic analysis was not performed, in this case; however, the two lesions are highly correlated, and a further definition was considered as of minor clinical relevance.
At hospital discharge, serum creatinine was 1.17 mg/dL with mild proteinuria (30 mg/dL). In the same year the patient's sister developed breast cancer and was identified as a carrier of the BRCA-2 mutation. However, the other family members, including our patient, preferred not to perform genetic testing for the BRCA mutation.
In January 2011 the patient was referred to our center. Glycemic control was good (glycated hemoglobin 6.5% on Repaglinide). Blood pressure was normal, without therapy. Cognitive impairment and psychomotor agitation, choreiform movements and intentional tremor, nystagmus and lower limb muscle weakness, hypotrophy and severe muscle wasting were present (height 155 cm, weight 36 Kg, BMI: 15). His speech was slow, slurred but coherent, and he appeared severely depressed. His last biochemical tests were: serum creatinine 2.1 mg/dL (eGFR 23 mL/min), proteinuria 3.6 g/24 hours, low-normal total proteins (6.2 g/dL) and normal serum albumin (3.7 g/dL). EKG was normal; no sign of cardiomyopathy was detected. Further tests showed: low IgG levels (499 mg/dL), normal IgA and IgM (213 and 115 mg/dL respectively); high PTH (445 pg/mL); moderate acidosis (pH 7.227; HCO3 22.8; SBE -3.7; normal lactates: 1.2 mmol/L); antinuclear antibodies and ANCA were negative.
Renal ultrasounds showed moderate medullary hyperechogeneity, consistent with tubulo-interstitial or vascular damage.
The rapid progression of kidney disease, with the development of nephrotic proteinuria, led us to review the samples of kidney tissue at a distance from the cancer lesions.
Of note, the changes were recorded before the onset of proteinuria and in the absence of hypertension, both at nephrectomy and over the follow-up.
Morphological examination revealed a widespread interstitial fibrosis and marked vascular changes characterized by intimal fibrosis of arcuate and interlobular arteries with a wedge-shaped area of interstitial fibrosis and tubular atrophy extending to the renal capsule suggestive of ischemic damage (Figure ). Hyaline arteriolosclerosis (Figures and ) and signs of chronic inflammation were also seen. These severe vascular lesions were the basis of the different glomerular alterations including ischemic and obsolescent glomeruli. The obsolescent glomeruli amounted to approximately 50% of the more than 100 glomeruli sampled. Some rare glomeruli (about 5-10%) showed focal segmental glomerulosclerosis, which in this context can be interpreted as consequent to the vascular alterations.
As the patient subsequently developed nephrotic syndrome, these lesions suggest that silent ischemic changes may result in the development of focal segmental glomerulosclerosis secondary to nephron loss, at least in some cases of MELAS-related nephropathy. | 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. | 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 41 years old.
The concentration of creatinine is 2.1 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 155.0 cm, which is 155.0 cm * 1 m / 100 cm = 1.55 m. The patient's weight is 36.0 kg. The patient's bmi is therefore 36.0 kg / (1.55 m * 1.55 m) = 14.984 kg/m^2.The patient's BMI is 15.0, indicating they are underweight.
Because the patient is underweight, we take the patient's weight, 36.0 kg as the patient's adjusted weight needed for the Cockroft-Gault Equation.
Using the Cockcroft-Gault equation:
CrCl = ((140 - age) * adjusted weight * gender_coefficient) / (serum creatinine * 72).
Plugging the patient's values gives us ((140 - 41) * 36.0 * 1) / (2.1 * 72) = 23.571 mL/min. Hence, the patient's creatinine clearance is 23.571 mL/min. | 23.571 |
{
"Calculator ID": 2,
"Calculator Name": "Creatinine Clearance (Cockcroft-Gault Equation)",
"Category": "lab test",
"Lower Limit": "19.0",
"Note ID": "pmc-8019405-1",
"Note Type": "Extracted",
"Relevant Entities": "{'sex': 'Male', 'weight': [54.5, 'kg'], 'height': [156.0, 'cm'], 'creatinine': [2.7, 'mg/dL'], 'age': [67, 'years']}",
"Row Number": 34,
"Upper Limit": "21.0"
} | medical_problem | A 67-year-old man in good health reported numbness and weakness of his lower legs in June 2010. He presented to the clinic due to the spread of the symptoms to his upper limbs. Magnetic resonance imaging revealed multiple lacuna infarctions. Laboratory analysis revealed anemia (hemoglobin [Hb], 9.8 g/dL) and renal dysfunction (creatine, 2.7 mg/dL). He was admitted to a nearby hospital for further examination and was diagnosed with hypertension and multiple mononeuropathy. In addition, laboratory findings revealed increased levels of C-reactive protein (CRP, 16.82 mg/dL). After 8 days in the hospital, severe right-flank pain suddenly occurred, and anemia worsened (Hb, 6.8 g/dL). Abdominal computed tomography (CT) without enhancement revealed a right perirenal hematoma. He was then transferred to our hospital for investigation and treatment.
On admission, his height was 156.0 cm, and his weight was 54.5 kg (approximately 2-kg loss over months). His blood pressure was 192/114 mm Hg; pulse, 98 bpm; and body temperature, 37.1 ℃. On physical examination, palpebral conjunctiva was pallid, and he had severe right-flank pain with muscular defense. No skin rush was evident in the extremities, although hypesthesia was detected by neurologic examination. Laboratory findings on admission are presented in Table . The results of the urine tests were as follows: protein levels, 2.4 g/g⋅Cr; occult blood 3+ by dipstick test; red blood cells ≧ 100/high-power field; and sediment contained granular cast 2+ . The results of serum examinations were as follows: white blood count, 13,610/µL (with 74.0% neutrophils and 16.0% eosinophils); hemoglobin, 6.2 g/dL; platelet count, 32.1 × 104/µL; alkaline phosphatase, 1,867 IU/L; γ-glutamyl transpeptidase (γ-GTP), 360 IU/L; blood urea nitrogen, 39 mg/dL; Cr, 1.3 mg/dL; erythrocyte sedimentation rate, 156 mm; C-reactive protein, 11.5 mg/dL; immunoglobulin (Ig) G, 2533 mg/dL; IgA, 306 mg/dL; IgM, 106 mg/dL; C3, 83 mg/dL; C4, 15 mg/dL; and CH50, 48 U/mL. ANA, PR3-ANCA, MPO-ANCA, anti-GBM antibody, and HBs-antigenemia were not detected. Contrast-enhanced CT revealed bilateral pleural effusion, right small renal infarction, and right perirenal hematoma. CT angiography revealed multiple small aneurysmal dilatations in the intrarenal branches of the bilateral renal arteries and the intrasplenic branches of the splenic artery (Fig. a–c). Emergency selective coil embolization was conducted to the right renal artery aneurysm, which was responsible for the bleeding (Fig. ). To obtain a definitive diagnosis, we performed a left sural nerve biopsy (Fig. ). We confirmed a small arterial occlusion with inflammatory cell infiltration in the sural nerve tissue, although a histological examination did not reveal fibrinoid necrosis or granuloma. Collectively, and based on his clinical and radiographic findings, we diagnosed polyarteritis nodosa.
On the fifth hospital day, we started oral prednisolone therapy at 40 mg/day. On the 8th and 15th hospital days, intravenous methylprednisolone pulse (500 mg/day) therapy was started for 3 consecutive days. Although these therapies suppressed the disease activity, including inflammatory response, urine protein, and pleural effusion, the patient failed to achieve remission. Intravenous pulse cyclophosphamide therapy was, therefore, given on the 30th day. Clinical symptoms such as numbness and weakness of limbs gradually diminished, and laboratory findings dramatically improved. Moreover, contrast-enhanced CT revealed the disappearance of pleural effusion and the decreased size of perirenal hematoma concomitant with aneurysms. The patient was then transferred to another hospital for rehabilitation training (Fig. ). | 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. | 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 67 years old.
The concentration of creatinine is 2.7 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 156.0 cm, which is 156.0 cm * 1 m / 100 cm = 1.56 m. The patient's weight is 54.5 kg. The patient's bmi is therefore 54.5 kg / (1.56 m * 1.56 m) = 22.395 kg/m^2.The patient's BMI is 22.4, 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 53.259 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) * 53.259 * 1) / (2.7 * 72) = 20.0 mL/min. Hence, the patient's creatinine clearance is 20.0 mL/min. | 20.0 |
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