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