Abnormal renal acidification in alcoholic liver disease.
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.
D000136:Acid-Base Equilibrium; D000141:Acidosis, Renal Tubular / Q000175:diagnosis*; D000328:Adult; D000437:Alcoholism / Q000150:complications*; D002122:Calcium Chloride; D002986:Clinical Trials as Topic; D006801:Humans; D007677:Kidney Function Tests; D008103:Liver Cirrhosis / Q000175:diagnosis / Q000652:urine; D008107:Liver Diseases / Q000175:diagnosis* / Q000652:urine; D008875:Middle Aged
D002122:Calcium Chloride