Frey, Felix J (2006). Impaired 11 beta-hydroxysteroid dehydrogenase contributes to renal sodium avidity in cirrhosis: hypothesis or fact? Hepatology, 44(4), pp. 795-801. Hoboken, N.J.: Wiley Interscience 10.1002/hep.21381
Full text not available from this repository. (Request a copy)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 11 beta-hydroxysteroid dehydrogenase type 2, an enzyme protecting the MR from promiscuous activation by cortisol in healthy mammalians.
Item Type: |
Journal Article (Further Contribution) |
|---|---|
Division/Institute: |
04 Faculty of Medicine > Department of Dermatology, Urology, Rheumatology, Nephrology, Osteoporosis (DURN) > Clinic of Nephrology and Hypertension |
UniBE Contributor: |
Frey, Felix (B) |
ISSN: |
0270-9139 |
ISBN: |
17006915 |
Publisher: |
Wiley Interscience |
Language: |
English |
Submitter: |
Factscience Import |
Date Deposited: |
04 Oct 2013 14:47 |
Last Modified: |
29 Mar 2023 23:32 |
Publisher DOI: |
10.1002/hep.21381 |
PubMed ID: |
17006915 |
Web of Science ID: |
000241338200003 |
URI: |
https://boris.unibe.ch/id/eprint/19778 (FactScience: 2721) |
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