The role of chronic anion gap and/or nonanion gap acidosis in the osteodystrophy of chronic renal failure in the predialysis era: a minority report.

Chronic renal failure (CRF) due to (1) glomerulopathies, vascular and tubulointerstitial disorders, and (2) chronic nonazotemic renal tubular disorders creates sustained acidosis in the untreated state. Number 1 represents a mixture of anion and nonanion gap acidosis and number 2 a pure nonanion gap acidosis. There remains significant uncertainty as to the role of the acidosis (CRF) in the associated osteodystrophy. In general, little attention has been given to this subject in recent monographs. It is the purpose of this review ('minority report') to 'reexamine' the information available on this subject in humans and animals. The author has concluded that the chronic metabolic acidosis of CRF may well contribute to the development and maintenance of the osteodystrophy, and that its treatment should be included along with the other modalities of therapy. The subject is not a 'dead issue' but one definitely deserving further investigation. The response of the skeleton to acid loads clearly represents another 'trade-off' in ion metabolism in CRF.