[Renal osteodystrophy: aluminium and secondary hyperparathyroidism]

Aluminium-related osteodystrophy results in osteomalacia or in the so-called aplastic bone. In this particular bone disease bone cells activities are distinctly reduced but there is no disorder of bone mineralization. Aluminium exerts a direct toxic effect on bone tissue, notably on osteoblasts which are always strongly depressed in case of major aluminium overload. Aluminium-related osteopathy is regularly accompanied by low levels of parathormone due to accumulation of aluminium in the parathyroid glands. Parathormone modulates the bone aluminium overload: hyperparathyroidism "protects" bones against the deleterious effect of aluminium, whereas aluminium deposit in bone increase after parathyroidectomy. The respective roles played by low parathormone levels and by aluminium deposits in aplastic bone lesions is difficult to determine since hypoparathyroidism itself can probably cause the aplastic osteopathy. The role of parathormone stands out more clearly now that in patients under dialysis the bone aluminium overload has markedly decreased. Many patients with aplastic bone (initially described in aluminium poisoning) show no aluminium deposits in bones but have, for some unknown reason, a normal or even low parathormone level. The clinical course of this type of osteopathy remains to be determined, but there seems to be no reason to worry since numerous patient are asymptomatic. Preventing secondary hyperparathyroidism while refraining from prescribing aluminium hydroxide is the principal therapeutic objective in osteodystrophy of haemodialysis patients.