Loss of bone resulting from accumulation of aluminum in bone of patients undergoing dialysis.

The effects of accumulation of aluminum on cancellous bone mass and histomorphometric parameters of bone formation and resorption are evaluated in three separate studies: a cross-sectional study in 120 patients receiving long-term maintenance dialysis, including patients with and without stainable bone aluminum; a longitudinal retrospective study in eight patients receiving hemodialysis, who had progressive accumulation of aluminum in bone. These patients had two bone biopsies 11 to 16 months apart; a longitudinal prospective study in 10 patients receiving long-term hemodialysis, who had histologically proved renal osteodystrophy and stainable bone aluminum. These patients were given deferoxamine for 9 to 12 months. Repeat bone biopsies were done thereafter, and decrease or disappearance of stainable bone aluminum was observed. The results of the independent studies demonstrate that aluminum accumulation in bone is associated not only with disturbed mineralization but also with loss of cancellous bone mass, and that removal of aluminum from bone results in gain in bone volume. The mechanisms of this phenomenon are related to a disproportionately greater effect of aluminum on bone formation than on bone resorption. The negative effect on bone formation is caused by decreased number and activity of osteoblasts, which is reversed by removal of aluminum from bone. In addition, the data show that aluminum induces suppression of bone turnover, with uncoupling between bone formation and resorption whereby the effects on bone formation exceed those on bone resorption. Thus, fractures in patients with renal failure and accumulation of aluminum may result not only from osteomalacia but also from osteopenia.