Primary aldosteronism (PA) is a group of disorders in which aldosterone is excessively produced. These disorders can lead to hypertension, hypokalemia, hypervolemia and metabolic alkalosis. The prevalence of PA ranges from 5% to 12% around the globe, and the most common causes are adrenal adenoma and adrenal hyperplasia. The importance of PA recognition arises from the fact that it can have a remarkably adverse cardiovascular and renal impact, which can even result in death. The aldosterone-to-renin ratio (ARR) is the election test for screening PA, and one of the confirmatory tests, such as oral sodium loading (OSL) or saline infusion test (SIT), is in general necessary to confirm the diagnosis. The distinction between adrenal hyperplasia (AH) or aldosteroneproducing adenoma (APA) is essential to select the appropriate treatment. Therefore, in order to identify the subtype of PA, imaging exams such as computed tomography or magnetic ressonance imaging, and/or invasive investigation such as adrenal catheterization must be performed. According to the subtype of PA, optimal treatment -surgical for APA or pharmacological for AH, with drugs like spironolactone and amiloride -must be offered.

We have carefully read the comments by Dr. Alain Gay [1] regarding our current review article, in which we describe the investigation and treatment options of primary aldosteronism [2]. Dr. Gay has questioned the statement about the more intense natriuretic effect of finerenone as compared to the other mineralocorticoid receptor antagonists (MRA). We characterized finerenone as having more natriuretic effects than spironolactone and eplerenone, as stated by other authors [3]. We appreciate Dr. Gay's comment and strongly agree that in the studies quoted, natriuresis was not an investigated parameter [4,5]. As a matter of fact, that statement was a speculation based on pharmacodynamics and pharmacokinetics studies that show finerenone to be >500-fold more selective for the mineralocorticoid receptor and to present a 3-10-fold higher potency and efficacy with IC50 (concentration of antagonist required to inhibit 50% activation of receptor) of 18 nmol/L [6,7].In healthy rats, the natriuretic activity of finerenone was tested as a head-to-head comparison of potency and efficacy with the steroidal MRA eplerenone. Both MRAs dose-dependently induced urinary sodium excretion. The application of 1 mg/kg finerenone resulted in similar natriuretic responses as 10 and 30 mg/kg eplerenone, whereas 10 mg/kg finerenone had a comparable natriuretic efficacy as 100 mg/kg eplerenone, suggesting that finerenone represents a more potent MRA [7,8].