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Subtypes of essential hypertension characterized by low renin levels allowed the identification of 2 different clinical entities: aldosterone-mediated mineralocorticoid receptor (MR) activation and cortisol-mediated MR activation.<\/jats:p>\n               <\/jats:sec>\n               <jats:sec>\n                  <jats:title>Evidence Acquisition<\/jats:title>\n                  <jats:p>This review is based upon a search of Pubmed and Google Scholar databases, up to August 2019, for all publications relating to endocrine hypertension, apparent mineralocorticoid excess (AME) and cortisol (F) to cortisone (E) metabolism.<\/jats:p>\n               <\/jats:sec>\n               <jats:sec>\n                  <jats:title>Evidence Synthesis<\/jats:title>\n                  <jats:p>The spectrum of cortisol-mediated MR activation includes the classic AME syndrome to milder (nonclassic) forms of AME, the latter with a much higher prevalence (7.1%) than classic AME but different phenotype and genotype. Nonclassic AME (NC-AME) is mainly related to partial 11\u03b2HSD2 deficiency associated with genetic variations and epigenetic modifications (first hit) and potential additive actions of endogenous or exogenous inhibitors (ie, glycyrrhetinic acid-like factors [GALFS]) and other factors (ie, age, high sodium intake) (second hit). Subjects with NC-AME are characterized by a high F\/E ratio, low E levels, normal to elevated blood pressure, low plasma renin and increased urinary potassium excretion. NC-AME condition should benefit from low-sodium and potassium diet recommendations and monotherapy with MR antagonists.<\/jats:p>\n               <\/jats:sec>\n               <jats:sec>\n                  <jats:title>Conclusion<\/jats:title>\n                  <jats:p>NC-AME has a higher prevalence and a milder phenotypical spectrum than AME. NC-AME etiology is associated to a first hit (gene and epigene level) and an additive second hit. NC-AME subjects are candidates to be treated with MR antagonists aimed to improve blood pressure, end-organ damage, and modulate the renin levels.<\/jats:p>\n               <\/jats:sec>","DOI":"10.1210\/clinem\/dgz315","type":"journal-article","created":{"date-parts":[[2020,1,7]],"date-time":"2020-01-07T17:32:43Z","timestamp":1578418363000},"page":"e924-e936","source":"Crossref","is-referenced-by-count":48,"title":["Classic and Nonclassic Apparent Mineralocorticoid Excess Syndrome"],"prefix":"10.1210","volume":"105","author":[{"ORCID":"https:\/\/orcid.org\/0000-0002-0668-412X","authenticated-orcid":false,"given":"Cristian A","family":"Carvajal","sequence":"first","affiliation":[{"name":"Department of Endocrinology, School of Medicine, Pontificia Universidad Cat\u00f3lica de Chile, Santiago, Chile"},{"name":"Millennium Institute on Immunology and Immunotherapy (IMII-ICM), Santiago, Chile"},{"name":"Centro Traslacional de Endocrinolog\u00eda UC (CETREN), Pontificia Universidad Catolica 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