Renal osteodystrophy

Uriel S. Barzel, Keith A. Hruska

Research output: Contribution to journalLetterpeer-review

3 Scopus citations


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.

Original languageEnglish
Pages (from-to)1428
Number of pages1
JournalNew England Journal of Medicine
Issue number21
StatePublished - Nov 23 1995


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