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Previous Volume 333:1428 November 23, 1995 Number 21 Next

	Since this article has no abstract, we have provided an extract of the first 100 words of the full text and any section headings.

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To the Editor: In their otherwise comprehensive review of the mechanisms of renal osteodystrophy, Hruska and Teitelbaum (July 20 issue)¹ do not mention the role of acidosis. The high-phosphate diet of the average adult American generates approximately 100 mmol of hydrogen ions daily. The inability of the failing kidney to excrete this endogenously produced acid results in metabolic acidosis, which stimulates osteoclastic bone resorption.^2,3 Thus, the skeleton, the principal source of alkali buffer, is slowly consumed in the defense against metabolic acidosis. This acid-induced bone resorption is present from the earlier stages of chronic renal failure but is overshadowed late . . . [Full Text of this Article]

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