Abstract

Evidence has emerged over the last several years indicating that aluminum accumulation in patients with chronic renal failure can cause certain forms of renal osteodystrophy, in particular osteomalacia and an aplastic lesion. The lines of evidence include epidemiological associations, chemical measurement and histological staining of bone aluminum, animal models of aluminum loading, and a favorable response to the removal of aluminum by chelation therapy. The primary sources of aluminum are dialysate solutions prepared from water with a high aluminum content and the oral ingestion of aluminum-containing phosphate binders. Desferrioxamine, a chelating agent with a high affinity for aluminum, can be used to remove aluminum during dialysis by increasing ultrafilterable plasma aluminum; preliminary results show that symptomatic patients markedly improve, both clinically and in their bone histology, after long-term chelation therapy with desferrioxamine. Treating water to ensure that aluminum levels are appropriately reduced in dialysate and the development of non-aluminum-containing phosphate binders are necessary to prevent aluminum-related osteodystrophy.

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