EXPERIMENTAL OSTEODYSTROPHY OF CHRONIC-RENAL-FAILURE INDUCED BY ALUMINUM-NITRILOTRIACETATE AND FERRIC-NITRILOTRIACETATE IN WISTAR RATS

The aluminum (Al) and iron (Fe) chelate complexes of nitrilotriacetate (NTA) cause renal insufficiency when they are administered intraperit oneally to rats. Their effects on bone metabolism were studied in 4 we ek old Wistar rats. Daily intraperitoneal administration of Al-NTA (3 mg Al/kg for 11 weeks) induced osteomalacia, impaired bone growth, dec reased bone mineral density, lower serum PTH levels than normal as wel l as renal insufficiency. Al staining showed diffuse deposition in the trabecula and a strong linear band of aluminum deposited at the miner alization front and along the cement line. The osteoid seen markedly w ithin the trabecula was probably the decalcified portion of the bone, the calcium apatite of which was defectively fabricated because of dif fuse Al deposition in the trabecula. Al deposition along the cement li ne would make it much more susceptible to external shear stress than n ormal. Although daily intraperitoneal administration of Fe-NTA (6 mg F e/kg for 11 weeks) caused impaired bone growth, decreased bone mineral content and renal insufficiency, the osteoid volume did not increase. Fe staining showed that Fe was deposited diffusely in the cytoplasm o f osteoblasts. The results of this study demonstrated that during rena l insufficiency, different minerals exhibit different modes of action on bone metabolism, and that Al-NTA is useful for experimental animal models of Al-induced osteomalacia in renal insufficiency.