Impaired 11β-hydroxysteroid dehydrogenase contributes to renal sodium avidity in cirrhosis: Hypothesis or fact?

Authors

  • Felix J. Frey

    Corresponding author
    1. Department of Nephrology and Hypertension, Inselspital, University of Berne, Switzerland
    • Department of Nephrology and Hypertension, Inselspital, University of Bern, Freiburgstrasse 10, CH-3010 Bern, Switzerland
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  • Potential conflict of interest: Nothing to report.

Abstract

Exaggerated renal sodium retention with concomitant potassium loss is a hallmark of cirrhosis and contributes to the accumulation of fluid as ascites, pleural effusion, or edema. This apparent mineralocorticoid effect is only partially explained by increased aldosterone concentrations. I present evidence supporting the hypothesis that cortisol confers mineralocorticoid action in cirrhosis. The underlying molecular pathology for this mineralocorticoid receptor (MR) activation by cortisol is a reduced activity of the 11β-hydroxysteroid dehydrogenase type 2, an enzyme protecting the MR from promiscuous activation by cortisol in healthy mammalians. (HEPATOLOGY 2006;44:795–801.)

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