16 patients with membranoproliferative glomerulonephritis had a mean serum chloride level significantly higher than that in normal subjects or in comparable groups of patients with nephrotic syndrome secondary to either systemic lupus erythematosus or to other primary nephrotic glomerular diseases. Differences in the severity of histologic alterations of the renal interstitium did not correlate with the different levels of serum chloride seen in these groups. The increased chloride concentration may be partially explained as a compensating reaction for a decrease in protein anions. However, a renal tubular acidifying defect demonstrated in one of our patients may also contribute to the hyperchloremia in some cases.