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?

1. A)Impaired renal 1α-hydroxylase activity leading to decreased calcitriol production
2. B)Autonomous parathyroid gland hyperfunction with excessive PTH secretion refractory to serum calcium suppressionGABARITO
3. C)Granulomatous production of calcitriol independent of PTH regulation
4. D)Excessive supplemental vitamin D intake causing increased intestinal calcium absorption
5. E)Thiazide diuretic-induced reduction in urinary calcium excretion