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Bone Disease in End-Stage Renal Failure

Marvin L. Daves, MD
JAMA. 1986;255(15):2025. doi:10.1001/jama.1986.03370150067019.
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To the Editor.—  Congratulations on the CONTEMPO '85 issue. This annual offering of a year's update on medical progress is a luxury. I write, however, to differ with Dr Glassock's conclusion, in the nephrology section, that aluminum is a primary factor in the bone complications of end-stage renal disease. The knowledge that phosphate depletion alone2,3 may cause rickets has been with us long enough to have been forgotten. Ingestion of aluminum hydroxide causes phosphate depletion.4 Thus, aluminum may mediate rickets (and osteomalacia) by causing phosphate depletion, rather than by poisoning the osteocyte.Reduction in bone formation caused by aluminum toxicity, as claimed by Dr Glassock, would have just the opposite result to what is known to happen when elemental phosphorus, lead, bismuth,5 or fluorine6 is the toxin. In these poisonings it is the osteoclastic activity of the osteocyte, not its osteoblastic activity, that is inhibited. At


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