Editorial: Diagnosis and Treatment of Primary Aldosteronism: from Clinical Origin to Translational Research

Abstract

Primary aldosteronism (PA) is one of the common causes of secondary hypertension, increasing the risk of cardiovascular disease and renal events as compared to essential hypertension, independently of blood pressure control (1-3).Primary aldosteronism (PA) is one of the common causes of secondary hypertension, and is associated with higher risks of cardiovascular, renal, and metabolic sequelae, including left ventricular hypertrophy, myocardial infarction, atrial fibrillation, stroke, microalbuminuria, osteoporosis, as well as metabolic syndrome (1,(4)(5)(6)(7).The present Research Topic highlights the interplay between clinical diagnosis, underlying genetic etiologies, and clinical outcome PA. Overall, it focuses on the histopathologic findings, gene mutation, the coexistence of cortisol, cosecretion, and targeted treatments of PA.Nanba et al. provide a template for researchers to study aldosterone-producing adrenal using formalin-fixed paraffin-material embedded sections for DNA capture, sequencing, and mutation determination.Although cortisol cosecretion in aldosterone-producing adenoma (APA) has been reported (8), the clinical relevance of such APA coexisting with cortisol-producing adenoma has not been illustrated (8). Inoue et al. summarize the current state of knowledge about cortisol cosecretion with PA. They conclude, there is increasing evidence about the relatively high prevalence of cortisol cosecretion in PA and its potential influence on adverse health outcomes.Adrenal venous sampling (AVS) is the test of choice to identify patients with a surgically curable subtype of PA (9). Okamoto et al. assess 1586 PA patients without apparent adrenal tumors in the multicenter study and conclude adrenal venous sampling should be considered for male hypokalemic PA patients with high ARRs because of the rates of the lateralized subtype and cardiovascular events are high in these patients.The major advance of understanding PA pathophysiology is the identification of several somatic driver mutations in ion channels and ATPases in lateralized aldosterone-producing adenoma (APA) (10). Utilizing the immunohistochemical (IHC) detection of aldosterone synthase (CYP11B2) has allowed the identification of aldosterone-producing cell clusters (APCCs) with unique focal localization positive for CYP11B2 expression in the subcapsular portion of the human adult adrenal cortex. Pauzi and Azizan reviewed APCCs associated aldosterone-stimulating somatic gene