A patient with chronic kidney disease has hyperphosphataemia, hypocalcaemia, and elevated PTH. The elevated PTH in this setting is most directly driven by:
- A Direct stimulation of parathyroid cells by phosphate
- B Increased FGF-23 directly stimulating parathyroid PTH secretion
- C Hypocalcaemia due to reduced renal 1-alpha hydroxylase activity decreasing calcitriol synthesis ✓
- D Metabolic acidosis of CKD directly increasing PTH gene transcription
Correct answer: C. Hypocalcaemia due to reduced renal 1-alpha hydroxylase activity decreasing calcitriol synthesis
Explanation
In CKD, reduced functional renal mass decreases 1-alpha-hydroxylase (CYP27B1) activity, reducing conversion of 25-OH-D to 1,25-OH2-D (calcitriol); deficient calcitriol reduces intestinal calcium absorption and fails to suppress PTH gene transcription, leading to secondary hyperparathyroidism. FGF-23 is elevated in CKD and suppresses 1-alpha-hydroxylase (worsening the deficiency) and reduces phosphate reabsorption, but does not directly stimulate PTH. Phosphate has indirect effects via FGF-23 and calcium.
Reference: Harper's Illustrated Biochemistry, 32nd ed.
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