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Orthopaedics · Metabolic bone disease: pathogenesis of renal osteodystrophy
Sample itemIn chronic kidney disease, which two changes are the main drivers of secondary hyperparathyroidism and renal bone disease?
Original practice item, not a recalled exam question. Nothing here is recorded.
The answer and the reasoning
D. Phosphate retention and reduced calcitriol synthesis
Failing kidneys retain phosphate and cannot make calcitriol, so intestinal calcium absorption falls. The resulting hypocalcaemia and phosphate retention stimulate parathyroid hormone secretion, causing high-turnover bone disease. FGF23 rises early as a compensatory response.
Option by option
A. Excess calcitriol and calcium retention
Calcitriol is reduced in CKD, not in excess.
B. Low phosphate and excess vitamin D receptor activity
Phosphate is retained, not low, in CKD.
C. High calcium with suppressed FGF23
Calcium tends to fall and FGF23 rises in CKD.
D. Phosphate retention and reduced calcitriol synthesis (correct)
Correct. Phosphate retention and calcitriol deficiency drive PTH secretion.
Source note: Original NextPrep sample item — pending expert review. This item is original practice material awaiting independent expert review, so confirm important facts in a standard textbook.
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