Chronic renal failure is the most common cause of stable chronic metabolic acidosis observed by the internist. So-called uremic acidosis has been believed to develop only in the later stages of progressive renal disease, when the serum creatinine level has risen above 4 mg/dL.1 Now Dr Widmer and associates tell us, in this issue of the Archives (see p 1099), that a slight but important rise in serum chloride level (4 mEq/L) and fall in serum bicarbonate level (6 mEq/L), with no change in anion gap, occurs early in chronic renal failure, when the serum creatinine level is in the range of 2 to 4 mg/dL. This non-anion gap, hyperchloremic metabolic acidosis was not, in contrast to the "clinical impression" held by some of us,2 a marker of tubulointerstitial, as compared with primary glomerular, disease.
These findings are most interesting but must be regarded as preliminary and requiring
Luke RG. Serum Chloride and Bicarbonate Levels in Chronic Renal Failure. Arch Intern Med. 1979;139(10):1091–1092. doi:10.1001/archinte.1979.03630470013006
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