In chronic renal failure, secondary hyperparathyroidism develops through which sequence of biochemical events?
- A Reduced GFR → calcitriol excess → inhibition of PTH → compensatory hyperplasia of C-cells
- B Reduced GFR → phosphate retention → hyperphosphataemia → hypocalcaemia + reduced renal 1-alpha-hydroxylase → low calcitriol → PTH secretion rises ✓
- C Reduced GFR → impaired magnesium excretion → hypermagnesaemia inhibiting PTH secretion → compensatory hyperparathyroidism
- D Reduced GFR → metabolic alkalosis → decreased ionised calcium → PTH secretion
Correct answer: B. Reduced GFR → phosphate retention → hyperphosphataemia → hypocalcaemia + reduced renal 1-alpha-hydroxylase → low calcitriol → PTH secretion rises
Explanation
In CKD, decreased GFR impairs phosphate excretion, causing hyperphosphataemia. Excess phosphate directly suppresses renal 1-alpha-hydroxylase and precipitates calcium, reducing ionised serum calcium. Simultaneously, reduced 1-alpha-hydroxylase activity decreases 1,25-(OH)2-D3 (calcitriol) production, impairing intestinal calcium absorption. Hypocalcaemia and low calcitriol both stimulate PTH secretion, causing secondary hyperparathyroidism with renal osteodystrophy. FGF-23 also plays a key role by suppressing 1-alpha-hydroxylase.
Reference: Harper's Illustrated Biochemistry, 32nd ed.
High-yield for: NEET PGINI-CETNExTFMGEUSMLEPLABMRCP
Written and medically reviewed by the StethoPrep medical team.