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.

中文翻译：

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肝脏疾病中钠和液体潴留的新机制

在肝病患者中，钠和液体潴留通常归因于有效血容量减少，从而刺激肾素-血管紧张素-醛固酮系统（RAAS）。然而，并非所有患者都表现出 RAAS 激活。新数据表明肝脏疾病中钠和液体潴留的潜在独立于醛固酮的机制。

研究人员得出结论，胆汁酸激活 ENaC 可能会导致肝脏疾病中的 Na ⁺和液体潴留。他们建议在临床管理中应考虑这种机制，特别是当对螺内酯缺乏反应时。