In patients with liver disease, sodium and fluid retention is often attributed to reduced effective blood volume, which stimulates the renin–angiotensin–aldosterone system (RAAS). However, not all patients show RAAS activation. New data suggest a potential aldosterone-independent mechanism of sodium and fluid retention in liver disease.

The researchers conclude that activation of ENaC by bile acids is likely to contribute to Na+ and fluid retention in liver disease. They suggest that this mechanism should be considered in clinical management, particularly when there is a lack of response to spironolactone.