Aluminium-related osteodystrophy and desferrioxamine treatment: role of phosphorus

We investigated (1) the prevalence of aluminium overload among96 patients with symptomatic bone disease haemodialysed from1987 to 1989 in the Sao Paulo area, Brazil; (2) the effect of6 months desferrioxamine (DFO) treatment (1–2 g/week).All patients underwent a first bone biopsy. Aluminium overload(extent of stainable bone aluminium more than 20% trabecularsurface) was observed in 74 of 96 patients. Forty overloadedpatients were divided into patients with high bone formationrate (BFR) (group 1; n=17) and patients with low BFR (group2; n=23), and had a second biopsy after DFO therapy. In bothgroups aluminium surface was reduced after treatment (P<0.001),osteoblast surface (P<0.02-P<0.01) and plasma parathyroidhormone (iPTH) (P<0.01) increased. In group 1 BFR remainedhigh. In group 2 BFR remained low in 16 patients (2a) and increasedin seven (P<0.02) (2b). In group 2a plasma phosphorus wasbelow that in group 2b patients, before (P<0.03) and after(P<0.01) DFO. The histological features of group 2a patientsresembled hypophos-phataemic osteomalacia, those of group 2bpatients aluminium osteodystrophy. These data show a high prevalence of aluminium overload in Brazilianpatients. Low-dose DFO therapy was safe, decreased bone pain,prevented fractures, and reduced stainable bone aluminium. Bonelesions only partially improved, suggesting that low phosphorusintake and/or plasma calcitriol concentrations may have preventedimprovement of bone formation and mineralization.