Renal osteodystrophy refers to the complex combination of skeletal abnormalities that develops in patients with longstanding chronic renal failure, with the potential to cause fractures and deformities. Management seeks to prevent these from occurring. Contributing elements include:
Osteomalacia
Osteomalacia - incomplete bone calcification caused by vitamin D deficiency. Rickets in children.
Caused by failure of the 1α-hydroxylation of vitamin D to form 1,25 dihydroxycholecalciferol, a step that usually occurs in renal tubular cells. Prevented by administration 1α-hydroxylated derivatives of vitamin D, (alfacalcidol or calcitriol). This raises serum calcium and also directly suppresses PTH secretion.
Hyperparathyroidism
Increased secretion of parathyroid hormone (PTH) is driven by hypocalcaemia (in part due to effective vitamin D deficiency) and high serum phosphate (as renal excretion is reduced). After some years, responsiveness of PTH to lowered phosphate and raised calcium levels is lost (tertiary hyperparathyroidism). Prevention is through control of calcium (see below) and phosphate levels (dietary modification and ingestion of phosphate binders such as calcium carbonate or acetate with food). Calciumsensor agonists are a more recent innovation.
Adynamic bone disease
Recognised more recently. Thought to be at least partially due to over-suppression of PTH by excessive use of vitamin D therapy. In the past aluminium toxicity (from dialysis and use of aluminium hydroxide as a phosphate binder) may have contributed to this.
This unusual combination of features makes standard methods for assessing bone density of very uncertain value in patients with chronic renal failure.
Further info
| Oedema << | >> Peritoneal dialysis |
