Abstract
Introduction: Several studies have now revealed the direct deleterious effects of excess aldosterone, especially in cardiovascular disease, independent of the usual effect of aldosterone on electrolyte transport [1,2]. These new pathologic findings appear to be direct effects of aldosterone on cardiovascular and other tissues, leading to tissue remodeling and fibrosis. Interestingly, very little attention has been directed toward the kidney and renal damage in primary aldosteronism (PA). In fact, only two publications from the same institution have examined renal function in PA in a limited approach, noting early microalbuminuria when compared to subjects with primary hypertension (PH) [3,4]. In general, studies of renal pathology in PA are lacking. This omission is quite surprising for a disease involving often severe hypertension, and given the new information on the direct effects of aldosterone on tissue fibrosis [5]. Recent knowledge holds that PA is a much more frequent cause of secondary hypertension than previously thought, being as high as 12% of all the hypertensive population, thus involving millions of individuals in the world, further increasing the demand for world organization of screening and evaluation protocols and high-standard special centers [6]. Further information on PA and renal function is mandatory, especially with the newer screening tests to monitor progression of chronic kidney disease (CKD) and the renoprotective features indicating that PA be part of the new tests in nephrology, such as urinary albumin excretion (UAE) and estimated glomerular filtration rate (GFR). The Primary Aldosteronism Prevalence in Italy (PAPY) study is a prospective survey of 1180 consecutive newly diagnosed hypertensive patients referred to specialized hypertension centers in Italy to detect the prevalence of PA and intensely study several of its characteristic features [7]. In this study, 490 subjects were deemed justified for an intensified evaluation for PA, aldosterone-producing adenomas (APA) were found in 4.8% of subjects, and idiopathic hyperaldosteronism (IHA) in 6.4%, for a total incidence of PA of 11.2% in the Italian hypertensive population [7]. The main feature examined for renal function was the UAE, but previous renal function studies also showed serum and urine hyperfiltration and increased microalbuminuria in PA; however, these studies were limited by size and the fact that they studied only patients with APA. As is also well known, increased UAE is a key determinant for cardiovascular damage and endothelial dysfunction in high-risk patients. Thus, UAE would also serve an important role in patients with PA as a marker of their overall cardiovascular burden.
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