Primary aldosteronism (PA) is a common cause of secondary hypertension (HT), characterized by the autonomous production of aldosterone by the adrenal glands. The excess of serum aldosterone not only increases blood pressure through sodium retention,1 but deleteriously affects the cardiovascular systems in both direct and indirect pathways, resulting in more cardiovascular events in patients with PA than in patients with essential HT.2, 3, 4 In general, PA is classified into two subtypes: unilateral PA, which includes aldosterone-producing adenoma (APA), or bilateral PA.5 Given that APA is curable by surgical resection of the tumor and has severe complications if not treated,6,7 it is imperative to understand the clinical features and pathogenesis of APA.

KCNJ5 is one of the most common somatic mutations of APAs which codes for a potassium channel in the adrenal gland and leads to the activation of calcium signal triggering aldosterone production.8, 9, 10 To date, ample evidence has shown the phenotypic features of KCNJ5-mutated APA, which included larger tumor size, younger age, higher plasma aldosterone levels, lower potassium levels, and larger response to endogenous adrenocorticotropic hormone (ACTH) than KCNJ5 wild-type APAs.8,11, 12, 13, 14, 15, 16 Moreover, some studies showed that surgical resection of KCNJ5-mutated APAs was associated with better recovery of cardiovascular damages, including left ventricular hypertrophy and arterial stiffness.17, 18, 19 However, the synthesized evidence is lacking about the potential burden of KCNJ5 mutation among patients with APAs due to a small sample size in each study, a variety of populations in each cohort, and different definitions and diagnostic procedures for PA.

Therefore, we aimed to provide updated summaries of the association between KCNJ5 mutation and cardiovascular outcomes including metabolic profiles, cardiovascular impairment, and the remission of HT after surgery. A better understanding of the potential burden of KCNJ5 mutation would provide clinical insight into the optimal management of patients with PA using genetic information.