Renal osteodystrophy: pathogenesis and management

Abstract

Several biochemical and hormonal abnormalities associated with renal insufficiency lead to complex disorders of bone which are described by the term renal osteodystrophy. Assessment of renal osteodystrophy in its early stages is primarily biochemical since symptoms generally do not occur until osteodystrophy is advanced. Therapy should be initiated early in the course of renal insufficiency in order to prevent the development of severe skeletal abnormalities. Foremost among the multiple factors involved in the pathogenesis of hyperparathyroidism are retention of phosphorus and low levels of calcitriol. The principal therapies for the prevention and treatment of hyperparathyroidism include the use of calcium salts taken with meals, as phosphorus binders, to prevent the absorption of phosphorus from the intestine, correction of acidosis and careful use of vitamin D metabolites such as calcitriol or 1-alpha-hydroxycholecalciferol. The prevalence of aluminum induced osteomalacia appears to be declining as aluminum salts have been replaced by calcium containing phosphate binders and there is increased attention to adequate water purification for dialysis. Other disorders such as adynamic bone and the accumulation of beta 2-microglobulin may require bone biopsy for accurate diagnosis and are more difficult to treat effectively.