Abnormal renal acidification in alcoholic liver disease.

Abstract

After ingestion of 150 mEq. of calcium chloride (CaCl-2), urinary acidification was studied for 6 hours in 22 normokalemic patients with alcoholic liver disease (L) of varying severity, and in 7 control (C) subjects during 10 studies. The degree of the induced systemic acidosis was similar in all groups. Nine L patients were unable to normally lower urine pH below 5.25 (L-I) and these were compared with the 13 L patients achieving lower pH (L-II) and with control subjects. This defect was consistently reproduced. Titratable acid excretion was less in L-I than in the other groups. The percentage contribution of ammonium to maximal net acid excretion was significantly higher in L-I and L-II than in C. No L-I patient had spontaneous metabolic acidosis, nor was there evidence of encephalopathy or of proximal tubular dysfunction. Sodium excretion was significantly lower in L-I than in either L-II or C. Sodium sulfate and sodium phosphate infused after acid-loading rapidly reduced urine pH into the appropriately acidic range in L-I patients with alcoholic liver disease by means of a simple, safe, and short acid-loading test. Although the mechanism of this renal tubular acidfying defect remains unknown a low distal delivery of sodium by limiting the transtubular potential difference may have been partially responsible.