Studies in patients on dialysis have shown that aluminum (A1) accumulation in bone plays a major role in the pathogenesis of osteomalacia. It has been suggested that deferoxamine (DFO) may be beneficial in the treatment of aluminum-induced osteomalacia. The present studies were performed in four groups of uremic rats to determine if DFO and/or discontinuation of A1 administration have an effect on bone histomorphometry and blood chemistries. The groups were: 1) uremic control 2) aluminum (0.75 to 1.0 mg/rat i.p., five times a week for twelve weeks): 3) aluminum + DFO, after twelve weeks A1 was discontinued and the rats received DFO (75 mg/rat two times a week for nine weeks); 4) aluminum + time, after twelve weeks A1 was discontinued and the rats were sacrificed after nine weeks. High levels of A1 in serum and bone and low levels of PTH were seen in rats receiving A1. Bone histology revealed A1 at the mineralization front, abnormal tetracycline uptake, and an increase in osteoid. DFO treatment did not significantly change the level of A1 in bone, however both DFO treatment and discontinuation of A1 reversed towards normal the above described lesions. In conclusion, these studies suggest that DFO and/or discontinuation of A1 administration to rats with approximately 30% of renal function greatly improve aluminum-induced osteomalacia.

Original languageEnglish
Pages (from-to)318-324
Number of pages7
JournalKidney International
Issue number3
StatePublished - 1986


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