title: Progress in aldosteronism: a review of the prevalence of primary aldosteronism in pre-hypertension and hypertension.
abstract: Primary aldosteronism (PA) secondary to excessive and/or autonomous aldosterone secretion from the renin-angiotensin system accounts for ∼10% of cases of hypertension and is primarily caused by bilateral adrenal hyperplasia (BAH) or aldosterone-producing adenomas (APAs). Although the diagnosis has traditionally been supported by low serum potassium levels, normokalaemic and even normotensive forms of PA have been identified expanding further the clinical phenotype. Moreover, recent evidence has shown that serum aldosterone correlates with increased blood pressure (BP) in the general population and even moderately raised aldosterone levels are linked to increased cardiovascular morbidity and mortality. In addition, aldosterone antagonists are effective in BP control even in patients without evidence of dysregulated aldosterone secretion. These findings indicate a higher prevalence of aldosterone excess among hypertensive patients than previously considered that could be attributed to disease heterogeneity, aldosterone level fluctuations related to an ACTH effect or inadequate sensitivity of current diagnostic means to identify apparent aldosterone excess. In addition, functioning aberrant receptors expressed in the adrenal tissue have been found in a subset of PA cases that could also be related to its pathogenesis. Recently a number of specific genetic alterations, mainly involving ion homeostasis across the membrane of zona glomerulosa, have been detected in ∼50% of patients with APAs. Although specific genotype/phenotype correlations have not been clearly identified, differential expression of these genetic alterations could also account for the wide clinical phenotype, variations in disease prevalence and performance of diagnostic tests. In the present review, we critically analyse the current means used to diagnose PA along with the role that ACTH, aberrant receptor expression and genetic alterations may exert, and provide evidence for an increased prevalence of aldosterone dysregulation in patients with essential hypertension and pre-hypertension.
authors.affiliation: Department of Endocrinology and Diabetes CenterG. Gennimatas Hospital, 154 Mesogion Avenue, 11527 Holargos, Athens, Greece andDepartment of PathophysiologyNational University of Athens, Mikras Asias 75, 11527 Athens, Greece edk-pgna@otenet.gr.
authors.forename: George
authors.initials: G
authors.lastname: Piaditis
authors.affiliation: Department of Endocrinology and Diabetes CenterG. Gennimatas Hospital, 154 Mesogion Avenue, 11527 Holargos, Athens, Greece andDepartment of PathophysiologyNational University of Athens, Mikras Asias 75, 11527 Athens, Greece.
authors.forename: Athina
authors.initials: A
authors.lastname: Markou
authors.affiliation: Department of Endocrinology and Diabetes CenterG. Gennimatas Hospital, 154 Mesogion Avenue, 11527 Holargos, Athens, Greece andDepartment of PathophysiologyNational University of Athens, Mikras Asias 75, 11527 Athens, Greece.
authors.forename: Labrini
authors.initials: L
authors.lastname: Papanastasiou
authors.affiliation: Department of Endocrinology and Diabetes CenterG. Gennimatas Hospital, 154 Mesogion Avenue, 11527 Holargos, Athens, Greece andDepartment of PathophysiologyNational University of Athens, Mikras Asias 75, 11527 Athens, Greece Department of Endocrinology and Diabetes CenterG. Gennimatas Hospital, 154 Mesogion Avenue, 11527 Holargos, Athens, Greece andDepartment of PathophysiologyNational University of Athens, Mikras Asias 75, 11527 Athens, Greece.
authors.forename: Ioannis I
authors.initials: II
authors.lastname: Androulakis
authors.affiliation: Department of Endocrinology and Diabetes CenterG. Gennimatas Hospital, 154 Mesogion Avenue, 11527 Holargos, Athens, Greece andDepartment of PathophysiologyNational University of Athens, Mikras Asias 75, 11527 Athens, Greece.
authors.forename: Gregory
authors.initials: G
authors.lastname: Kaltsas
mesh_terms: D000324:Adrenocorticotropic Hormone / Q000378:metabolism; D006801:Humans; D006929:Hyperaldosteronism / Q000150:complications* / Q000175:diagnosis / Q000453:epidemiology* / Q000235:genetics; D006973:Hypertension / Q000150:complications* / Q000453:epidemiology* / Q000235:genetics; D058246:Prehypertension / Q000150:complications* / Q000453:epidemiology* / Q000235:genetics; D015995:Prevalence
chemical_list: D000324:Adrenocorticotropic Hormone