Effects of systemic aluminum on the resolution of a uremic and dietary phosphorus-dependent model of uremic osteomalacia in rats.

We have developed a model of osteomalacia that is dependent on both uremia and the feeding of a diet low in phosphorus and that can be reversed by subsequent dietary phosphorus repletion. The objectives for this study were to use this model to investigate the role of aluminum (Al) in both the induction and resolution of osteomalacia. Adult male Sprague-Dawley rats were five-sixths nephrectomized and fed either low or normal dietary phosphorus, both with and without intraperitoneal Al injections. Uremic rats fed low phosphorus developed osteomalacia characterized by increased osteoid surface, volume, and thickness and osteoid maturation time and decreased mineralizing surface. Al-treated uremic rats fed low phosphorus were similarly affected, developing increased osteoid volume and thickness and osteoid maturation time and decreased osteoblastic surface, mineralizing surface, and bone formation rate. In addition, they had a significantly increased Al-positive surface. Al-treated uremic rats fed normal phosphorus had only increased osteoid thickness and aluminum-positive surface and decreased osteoblastic surface. Osteomalacic rats continuously treated with Al during the induction and phosphorus repletion stages had increased growth plate thickness, osteoid volume and thickness, and Al-positive surface and decreased osteoblastic and mineralizing surface. Mineralization in these rats was impaired to such a degree that no detectable double labels were present. Osteomalacic rats treated with Al during the induction phase but not during phosphorus repletion had increased osteoid surface and volume and Al-positive surface and decreased osteoblastic and mineralizing surface. Double labels were not detectable in these rats, either.(ABSTRACT TRUNCATED AT 250 WORDS)