{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,1]],"date-time":"2026-10-01T02:24:18Z","timestamp":1790821458094,"version":"4.1.0"},"reference-count":0,"publisher":"Georg Thieme Verlag KG","issue":"02\/03","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["Exp Clin Endocrinol Diabetes"],"published-print":{"date-parts":[[2019,2]]},"abstract":"<jats:title>Abstract<\/jats:title><jats:p>Primary aldosteronism is a common cause of endocrine hypertension. It results from the excess production of aldosterone by the adrenal cortex and is related to increased morbidity and mortality. Most cases of PA are sporadic but inherited patterns of the disease have been reported in the literature. Four forms of familial hyperaldosteronism (FH-I- FH-IV) are currently recognized, and the genetic basis has been clarified in recent years. In FH-I patients, aldosterone excess is produced by a CYP11B1\/CYP11B2 fusion gene and it is suppressed by glucocorticoid treatment. FH-II is caused by mutations in the inwardly rectifying chloride channel CLCN2. FH-III is caused by mutations in KCNJ5, a gene coding for an inward rectifier K+ channel and mutations in the T-type calcium channel subunit CACNA1H cause FH-IV. In this review we summarize the knowledge on inherited forms of primary aldosteronism, the genetic alterations that cause them and the implications it may have for the classification. Based on current evidence, we propose the term \u201cfamilial hyperaldosteronism\u201d to refer only to inherited forms of primary aldosteronism with a known genetic basis.<\/jats:p>","DOI":"10.1055\/a-0713-0629","type":"journal-article","created":{"date-parts":[[2018,9,10]],"date-time":"2018-09-10T22:50:22Z","timestamp":1536619822000},"page":"93-99","source":"Crossref","is-referenced-by-count":21,"title":["Inherited Forms of Primary Hyperaldosteronism: New Genes, New Phenotypes and Proposition of A New Classification"],"prefix":"10.1055","volume":"127","author":[{"given":"Luis","family":"Perez-Rivas","sequence":"additional","affiliation":[{"name":"Medizinische Klinik und Poliklinik IV, Ludwig Maximilian University, Munich, Germany"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Tracy","family":"Williams","sequence":"additional","affiliation":[{"name":"Medizinische Klinik und Poliklinik IV, Ludwig Maximilian University, Munich, Germany"},{"name":"Division of Internal Medicine and Hypertension, Department of Medical Sciences, University of Turin, Turin, Italy"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Martin","family":"Reincke","sequence":"additional","affiliation":[{"name":"Medizinische Klinik und Poliklinik IV, Ludwig Maximilian University, Munich, Germany"}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"194","published-online":{"date-parts":[[2018,9,10]]},"container-title":["Experimental and Clinical Endocrinology &amp; Diabetes"],"original-title":[],"language":"en","link":[{"URL":"http:\/\/www.thieme-connect.de\/products\/ejournals\/pdf\/10.1055\/a-0713-0629.pdf","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2019,2,27]],"date-time":"2019-02-27T23:48:34Z","timestamp":1551311314000},"score":1,"resource":{"primary":{"URL":"http:\/\/www.thieme-connect.de\/DOI\/DOI?10.1055\/a-0713-0629"}},"subtitle":[],"short-title":[],"issued":{"date-parts":[[2018,9,10]]},"references-count":0,"journal-issue":{"issue":"02\/03","published-online":{"date-parts":[[2019,2,27]]},"published-print":{"date-parts":[[2019,2]]}},"URL":"https:\/\/doi.org\/10.1055\/a-0713-0629","relation":{},"ISSN":["0947-7349","1439-3646"],"issn-type":[{"value":"0947-7349","type":"print"},{"value":"1439-3646","type":"electronic"}],"subject":[],"published":{"date-parts":[[2018,9,10]]}}}