ALUMINUM-RELATED OSTEODYSTROPHY AND DESFERRIOXAMINE TREATMENT - ROLE OF PHOSPHORUS

We investigated (1) the prevalence of aluminium overload among 96 pati ents with symptomatic bone disease haemodialysed from 1987 to 1989 in the Sao Paulo area, Brazil; (2) the effect of 6 months desferrioxamine (DFO) treatment (1-2 g/week). All patients underwent a first bone bio psy. Aluminium overload (extent of stainable bone aluminium more than 20% trabecular surface) was observed in 74 of 96 patients. Forty overl oaded patients were divided into patients with high bone formation rat e (BFR) (group 1; n = 17) and patients with low BFR (group 2; n = 23), and had a second biopsy after DFO therapy. In both groups aluminium s urface was reduced after treatment (P < 0.001), osteoblast surface (P < 0.02-P < 0.01) and plasma parathyroid hormone (iPTH) (P < 0.01) incr eased. In group 1 BFR remained high. In group 2 BFR remained low in 16 patients (2a) and increased in seven (P<0.02) (2b). In group 2a plasm a phosphorus was below that in group 2b patients, before (P<0.03) and after (P<0.01) DFO. The histological features of group 2a patients res embled hypophosphataemic osteomalacia, those of group 2b patients, alu minium osteodystrophy. These data show a high prevalence of aluminium overload in Brazilian patients. Low-dose DFO therapy was safe, decreas ed bone pain, prevented fractures, and reduced stainable bone aluminiu m. Bone lesions only partially improved, suggesting that low phosphoru s intake and/or plasma calcitriol concentrations may have prevented im provement of bone formation and mineralization.