Aluminum: effects on bone and role in the pathogenesis of renal osteodystrophy

Renal osteodystrophy is a complex disorder that can produce a variety of histologic changes in bone. Classically, excess parathyroid hormone (PTH) secretion in patients with chronic renal failure leads to the development of skeletal lesions characterized by increases in bone cell activity and by high rates of bone formation and turnover. In contrast, aluminium retention in the body in those undergoing long-term dialysis is often associated with diminished bone cell activity and bone formation. In some patients with renal osteodystrophy, both pathogenic factors may be operative. Thus the histologic features in an individual patient can represent the combined manifestations of both excess PTH secretion and bone aluminum toxicity; the relative roles of each of these two pathogenic processes must be carefully evaluated. In the current review, several pathophysiologic mechanisms of aluminum toxicity in bone are summarized.