Aluminium-related osteodystrophy and desferrioxamine treatment: role of phosphorus

Abstract

We investigated (1) the prevalence of aluminium overload among 96 patients with symptomatic bone disease haemodialysed from 1987 to 1989 in the Sao Paulo area, Brazil; (2) the effect of 6 months desferrioxamine (DFO) treatment (1-2g/week). All patients underwent a first bone biopsy. Aluminium overload (extent of stainable bone aluminium more than 20% trabecular surface) was observed in 74 of 96 patients. Forty overloaded patients were divided into patients with high bone formation rate (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 surface was reduced after treatment (P < 0.001), osteoblast surface (P < 0.02-P < 0.01) and plasma parathyroid hormone (iPTH) (P < 0.01) increased. 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 plasma 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 resembled hypophosphataemic osteomalacia, those of group 2b patients aluminium osteodystrophy. These data show a high prevalence of aluminium overload in Brazilian patients. Low-dose DFO therapy was safe, decreased bone pain, prevented fractures, and reduced stainable bone aluminium. Bone lesions only partially improved, suggesting that low phosphorus intake and/or plasma calcitriol concentrations may have prevented improvement of bone formation and mineralization.

Hypokinetic azotemic osteodystrophy

“…This result suggested that the removal of aluminum partially restores the gland's sensitivity. This finding is also supported by another clinical study carried out after 6 months of continuous deferoxamine administration [19].…”

“…Aluminum toxicity, the main cause of low-bone-turnover osteomalacia in the 1970s and 1980s, is now better managed in most developed countries [16]. In other areas of the world [17][18][19], however, aluminum toxicity remains a major challenge. The change in the pattern of aluminum exposure alone cannot explain the increase in the prevalence of adynamic bone disease.…”

Intoxicação alumínica na DRC

“…43 O controle do tratamento pode ser feito por meio do teste de desferroxamina ou da biópsia óssea. [44][45][46] …”

Improvement of adynamic bone disease after renal transplantation

“…The bone specimens were fixed in 70% ethanol and processed for histomorphometry as previously described (7). For aluminum quantification, the material was stained with aurin tricarboxylic acid.…”