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).
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.