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Marvin L. Daves, MD
University of Colorado Medical School Denver

JAMA. 1986;255(15):2025.

	Since this article does not have an abstract, we have provided the first 150 words of the full text PDF and any section headings.

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 alone^2,3 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 . . . [Full Text PDF of this Article]

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