Spironolactone-Induced Hyperchloremic Acidosis in Cirrhosis

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Abstract

Six patients with alcoholic cirrhosis developed a reversible metabolic acidosis during treatment with the aldosterone antagonist spironolactone. Mean serum bicarbonate concentration decreased significantly with spironolactone therapy (100 to 200 mg/day) from 18.2 ± 4.5 to 10.9 ± 3.2 meq/litre (P < 0.001). Upon withdrawal of spironolactone, serum bicarbonate concentration increased from 10.9 ± 3.2 to 18.1 ± 3.5 meq/litre (P < 0.001). During the development of this hyperchloremic metabolic acidosis, serum potassium concentration rose from 3.7 ± 0.5 to 5.0 ± 0.8 meq/litre (P < 0.005); this reversed after cessation of spironolactone therapy. These effects of spironolactone treatment were not associated with significant alterations in serum creatinine or sodium concentration. Thus, even though an aldosterone antagonist in the treatment of sodium and water retention in cirrhotic patients may prevent hypokalemia and rapid diuresis, it may also induce or worsen another complication: hyperchloremic metabolic acidosis.

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