• H Koch, H Reich, D Franke, and G Delling.
• Monatsschr Kinderh. 1986 May 1; 134 (5): 279-81.

AbstractAn infant with uremia due to congenital renal hypoplasia was treated with oral aluminum hydroxide for 9 months in an attempt to reduce hyperphosphatemia. An increasingly painful osteopathy with pathological fractures ensued with loss of thoracic wall stability and respiratory failure. Increased serum aluminium levels and histochemically proved deposits of aluminium at the mineralisation front between calcified and noncalcified osteoid were demonstrated. In the context of recent findings concerning aluminium bone toxicity it is beyond doubt that this phosphate binding agent was detrimental for this child. Though a low phosphate diet normalized hyperphosphatemia after aluminium hydroxide treatment had been stopped, no effect on the progressive osteopathy was observed. Since aluminium hydroxide as a phosphate binder can be replaced by calcium carbonate or a low phosphate diet at least in young children, it should not be further recommended in this age group. This seems especially important in nondialyzed patients.

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