In patients with severe chronic renal failure (SCRF), especially in those undergoing chronic dialysis, aluminium may accumulate in the body. The aluminium is derived from the dialysate and/or from orally-administered, aluminium-containing phosphate binders. Accumulation preferentially occurs in the bone causing aluminium-induced osteomalacia. The physiopathological mechanisms of the disease still have to be elucidated. It has been suggested that aluminium accumulates at the osteoid/calcified-bone boundary (OCBB) inhibiting the influx of calcium there, and also that aluminium directly suppresses the secretion of parathyroid hormone (PTH). A third factor inducing the mineralization defect may be the presence of aluminium within the mitochondria of the osteoblast. In accordance with these hypotheses, hypercalcemia and relatively low iPTH levels are frequently found in aluminium-induced osteomalacia. Histologic methods are essential for demonstrating the actual existence of aluminium-induced osteomalacia. A large bone biopsy is desirable. When the biopsy is not decalcified and embedded in plastic, excellent histologic pictures are obtained wherein mineralized and non-mineralized bone (i.e. osteoid) can be distinguished clearly. Furthermore, the un-decalcified sections can be stained for aluminium, iron or both, and they are suitable for evaluation of the bone marrow status. Several features, like irregularly distributed osteoid with variable thickness, a relatively low number of cubic osteoblasts, and the absence of marrow fibrosis, are suggestive of aluminium-induced osteomalacia. However, the latter can only be proven by histochemical methods, e.g. by the aluminon staining. The treatment of aluminium-induced osteomalacia is quite different from that of other types of renal bone disease.(ABSTRACT TRUNCATED AT 250 WORDS)