A 46-year-old woman with chronic kidney disease on dialysis has a calcium of 8.9 mg/dL, phosphate of 6.8 mg/dL, and intact PTH of 1200 pg/mL. She has pruritus, bone pain, and radiological subperiosteal resorption. Cinacalcet and phosphate binders have failed. What is the underlying mechanism of her condition?
- A Autonomous adenoma formation independent of serum calcium
- B Phosphate retention and calcitriol deficiency causing chronic parathyroid stimulation ✓
- C Loss of calcium-sensing receptor function limited to the kidney
- D Excess dietary calcium intake suppressing vitamin D activation
Explanation
Secondary hyperparathyroidism of chronic kidney disease results from phosphate retention, reduced renal calcitriol production with impaired intestinal calcium absorption, and hypocalcaemia, all of which chronically drive parathyroid hyperplasia. In advanced cases nodular hyperplasia becomes autonomous, termed tertiary hyperparathyroidism, and subtotal or total parathyroidectomy with autotransplantation is indicated when medical therapy fails. Option A describes a single adenoma, which characterises primary rather than secondary disease.
Reference: Harrison's Principles of Internal Medicine, 21st ed.
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Written and medically reviewed by the StethoPrep medical team.