Renal Tubular Acidosis in Cirrhosis

Of 15 patients with hepatic cirrhosis in whom renal acid excretion and potassium conservation were studied, urinary pH fell normally after acid loading in four, and the response was borderline in two and clearly abnormal in nine. Blood pH before acid loading and total hydrogen ion excretion after acidification were normal in most patients. However, titratable acidity of urine was reduced, and ammonium excretion increased. Two patients had a more severe defect with low rates of total hydrogen ion excretion and "spontaneous" metabolic acidosis. Impaired renal potassium conservation accompanied the acidification abnormality in six patients. Hypercalciuria was present in two, and renal glycosuria in one. The coexistence of renal tubular acidosis and cirrhosis may explain why some cirrhotic patients readily become hypokalemic and remain so despite treatment with potassium salts. Renal tubular acidosis, through its effects on ammonium metabolism, may also make some patients susceptible to recurrent episodes of hepatic precoma.