Electrolyte Disorders USMLE Step 1 Practice Question
A 52-year-old man with a 12-year history of stage 4 chronic kidney disease (eGFR 18 mL/min/1.73m²) presents to clinic with progressive nausea, constipation, and nocturia. He has been on hemodialysis three times weekly for the past 2 years. Vital signs are stable. Laboratory values show: corrected serum calcium 11.8 mg/dL (normal 8.5-10.5), phosphate 6.2 mg/dL (normal 2.5-4.5), intact PTH 420 pg/mL (normal 10-65), and magnesium 2.1 mEq/L (normal 1.7-2.2). Serum 25-hydroxyvitamin D is normal. He denies use of vitamin D supplements, thiazide diuretics, or over-the-counter antacids. There is no history of sarcoidosis or tuberculosis. Which of the following best explains the pathophysiology of his hypercalcemia?
Answer choices
- AImpaired renal 1α-hydroxylase activity leading to decreased calcitriol production
- BAutonomous parathyroid gland hyperfunction with excessive PTH secretion refractory to serum calcium suppressionCorrect answer
- CGranulomatous production of calcitriol independent of PTH regulation
- DExcessive supplemental vitamin D intake causing increased intestinal calcium absorption
- EThiazide diuretic-induced reduction in urinary calcium excretion
- FMilk-alkali syndrome from calcium-based phosphate binder use
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