Among edematous disorders, liver cirrhosis (LC) is considered one of the main models of secondary hyperaldosteronism (SH), as pointed out by several studies in the past [1]. Aldosterone is expected to be increased in patients with liver disease when pH occurs. The RAAS may also be implicated in the onset and progression of liver fibrosis. Since the etiology of cirrhosis and its treatments have profoundly changed over the years we aimed to evaluate the presence and severity of secondary hyperaldosteronism in patients with ACLD or mild pH.
