What is it about?
Hormones that regulate body fluids through actions in the kidney have long been thought to be responsible for sodium and fluid retention in liver disease. We thought that bile acids, which are made by the liver, but can end up in the urine in liver disease, might independently increase the activity of sodium channels in the kidney. We tested the idea of hormone-independent fluid retention by blocking the key hormone aldosterone in a mouse model of liver disease. Despite not seeing an increase in the number of sodium channels as would be expected with aldosterone and other hormones, we nevertheless saw increased sodium and fluid retention in these mice. When we dissected the kidney and tested the effect of bile acids on sodium channels, we found that bile acids made the channels that were already present more active.
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Why is it important?
Despite the current thought that mis-regulation of volume hormones during liver disease is responsible for fluid retention in liver disease, it has long been proposed that other mechanisms exist. Our study provides evidence for an alternative mechanism, and provides a rationale for alternative strategies to treat patients.
Perspectives
Working on this study was rewarding as it helps establish the physiological importance of an effect (bile acid activation of the epithelial sodium channel) we had only previously seen outside of an animal. It may also help explain poorly understood observations in previous studies.
Ossama Kashlan
University of Pittsburgh
Read the Original
This page is a summary of: Epithelial Na+ Channel Activation after Bile Duct Ligation with Mineralocorticoid Receptor Blockade, Journal of the American Society of Nephrology, July 2024, Wolters Kluwer Health,
DOI: 10.1681/asn.0000000000000442.
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