Abstract

The main forms of renal osteodystrophy are secondary hyperparathyroidism, aluminum-induced bone disease and adynamic bone disease without aluminum intoxication. Aluminum intoxication has become rare because of control of the dialysate solution and avoidance of aluminum containing phosphate binders. Secondary hyperparathyroidism still develops early in the course of renal failure and remains the most frequent form of osteodystrophy in patients treated by maintenance hemodialysis. Several factors, including hyperphosphatemia and deficient synthesis of 1,25-dihydroxyvitamin D are involved in its pathogenesis. Secondary hyperparathyroidism is symptomatic only in severely affected patients. Prevention depends on control of serum phosphorus +/- prescription of 1-alpha-hydroxylated vitamin D derivatives or may require subtotal parathyroidectomy when hyperparathyroidism is refractory.Adynamic bone disease not related to aluminum intoxication has been increasingly recognized in recent years and is presently the most frequent form of osteodystrophy in continuous ambulatory peritoneal dialysis patients. This condition, characterized by low bone turnover and depression of bone formation, appears to be associated with an increased risk of bone fracture. The main pathophysiologic feature is excessive treatment of hyperparathyroidism leading to hypoparathyroidism. Serum immunoreactive 1,84-parathormone levels should therefore be kept at a level of 1.5-fold to 3-fold the upper limit of normal in patients treated by maintenance hemodialysis.

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