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Spironolactone-Induced Hyperchloremic Acidosis in Cirrhosis

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▸Requests for reprints should be addressed to Patricia A. Gabow, M.D.; Denver General Hospital, West 8th Avenue and Cherokee Street; Denver, CO 80204.

Denver, Colorado

© 1979 American College of PhysiciansAmerican College of Physicians

Ann Intern Med. 1979;90(3):338-340. doi:10.7326/0003-4819-90-3-338
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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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