Chronic kidney disease-mineral and bone disorder
Effect · PO4 up Calcitriol down
The failing kidney can neither excrete phosphate nor make calcitriol. FGF23 rises first, then PTH; calcium falls; and the combination produces renal osteodystrophy and vascular calcification.
Traced from the start
- Fall in ionised calciumRise in ionised calcium
- Calcium-sensing receptor on parathyroid chief cells
- Phosphate load and hyperphosphataemia
- Osteocyte phosphate sensing
- Cholecalciferol from skin and diet
- Hepatic 25-hydroxylation
- Parathyroid hormoneFibroblast growth factor 2325-hydroxyvitamin D (calcifediol)
- Renal proximal tubule: 1-alpha-hydroxylaseRenal proximal tubule: phosphate handling
- Chronic kidney disease-mineral and bone disorder
Detail
- Sequence
- FGF23 rises earliest, then calcitriol falls, then PTH rises; frank hyperphosphataemia and hypocalcaemia appear late, usually once eGFR is below about 30 mL/min
- Biochemistry
- Phosphate high, calcitriol low, calcium low or normal, PTH high, FGF23 high, alkaline phosphatase high
- Bone
- High-turnover osteitis fibrosa from PTH excess, or adynamic bone disease when PTH is over-suppressed by calcium-based binders and active vitamin D; osteomalacia if vitamin D is also deficient
- Treatment
- Dietary phosphate restriction, non-calcium binders (sevelamer, lanthanum), active vitamin D analogues, and cinacalcet for persistent hyperparathyroidism
When it goes wrong
Dialysis patient with a high calcium-phosphate product
Vascular and valvular calcification, and calciphylaxis: painful necrotic skin ulcers with a high mortality
Over-suppression of PTH in a dialysis patient
Adynamic bone disease: low turnover, fractures, and a greater tendency to hypercalcaemia and to vascular calcification
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