{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,1]],"date-time":"2026-10-01T00:51:57Z","timestamp":1790815917969,"version":"4.1.0"},"reference-count":70,"publisher":"Oxford University Press (OUP)","issue":"3","content-domain":{"domain":["eje.bioscientifica.com"],"crossmark-restriction":true},"short-container-title":[],"published-print":{"date-parts":[[2018,3]]},"abstract":"<jats:p>Aldosterone is the main mineralocorticoid hormone in humans and plays a key role in maintaining water and electrolyte homeostasis. Primary aldosteronism (PA), characterized by autonomous aldosterone overproduction by the adrenal glands, affects 6% of the general hypertensive population and can be either sporadic or familial. Aldosterone-producing adenoma (APA) and bilateral adrenal hyperplasia (BAH) are the two most frequent subtypes of sporadic PA and 4 forms of familial hyperaldosteronism (FH-I to FH-IV) have been identified. Over the last six years, the introduction of next-generation sequencing has significantly improved our understanding of the molecular mechanisms responsible for autonomous aldosterone overproduction in both sporadic and familial PA. Somatic mutations in four genes (<jats:italic>KCNJ5, ATP1A1, ATP2B3<\/jats:italic> and <jats:italic>CACNA1D<\/jats:italic>), differently implicated in intracellular ion homeostasis, have been identified in nearly 60% of the sporadic APAs. Germline mutations in <jats:italic>KCNJ5<\/jats:italic> and<jats:italic> CACNA1H<\/jats:italic> cause FH-III and FH-IV, respectively, while germline mutations in <jats:italic>CACNA1D<\/jats:italic> cause the rare PASNA syndrome, featuring primary aldosteronism seizures and neurological abnormalities. Further studies are warranted to identify the molecular mechanisms underlying BAH and FH-II, the most common forms of sporadic and familial PA whose molecular basis is yet to be uncovered.<\/jats:p>","DOI":"10.1530\/eje-17-0946","type":"journal-article","created":{"date-parts":[[2018,1,19]],"date-time":"2018-01-19T01:35:12Z","timestamp":1516325712000},"page":"R101-R111","update-policy":"https:\/\/doi.org\/10.1530\/crossmarkpolicy-1","source":"Crossref","is-referenced-by-count":49,"title":["GENETICS IN ENDOCRINOLOGY: The expanding genetic horizon of primary aldosteronism"],"prefix":"10.1093","volume":"178","author":[{"given":"Silvia","family":"Monticone","sequence":"first","affiliation":[{"name":"1Division of Internal Medicine and Hypertension Unit, Department of Medical Sciences, University of Torino, Torino, Italy"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Fabrizio","family":"Buffolo","sequence":"additional","affiliation":[{"name":"1Division of Internal Medicine 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analysis of remission rates in an international cohort","volume":"5","year":"2017","journal-title":"Lancet Diabetes Endocrinology"},{"key":"ref311","doi-asserted-by":"crossref","first-page":"4290","DOI":"10.1210\/jc.2016-1504","article-title":"A novel phenotype of familial hyperaldosteronism type III: concurrence of aldosteronism and Cushing\u2019s syndrome","volume":"101","year":"2016","journal-title":"Journal of Clinical Endocrinology and Metabolism"},{"key":"ref91","doi-asserted-by":"crossref","first-page":"111","DOI":"10.1016\/j.mce.2013.11.022","article-title":"Development of monoclonal antibodies against human CYP11B1 and CYP11B2","volume":"383","year":"2014","journal-title":"Molecular and Cellular Endocrinology"},{"key":"ref241","doi-asserted-by":"crossref","first-page":"74","DOI":"10.1016\/j.mce.2016.10.025","article-title":"Disordered zonal and cellular CYP11B2 enzyme expression in familial hyperaldosteronism type 3","volume":"439","year":"2017","journal-title":"Molecular and 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aldosteronism","volume":"31","year":"1998","journal-title":"Hypertension"},{"key":"ref491","doi-asserted-by":"crossref","first-page":"129","DOI":"10.1161\/HYPERTENSIONAHA.117.09057","article-title":"Aldosterone-producing adenomas: histopathology-genotype correlation and identification of a novel CACNA1D mutation.","volume":"70","year":"2017","journal-title":"Hypertension"},{"key":"ref111","first-page":"1109","article-title":"Hypertension, increased aldosterone secretion and low plasma renin activity relieved by dexamethasone","volume":"95","year":"1966","journal-title":"Canadian Medical Association Journal"},{"key":"ref141","doi-asserted-by":"crossref","first-page":"462","DOI":"10.1210\/endo-115-2-462","article-title":"Receptor binding and biological activity of 18-hydroxycortisol","volume":"115","year":"1984","journal-title":"Endocrinology"},{"key":"ref421","doi-asserted-by":"crossref","first-page":"857","DOI":"10.1038\/jhh.2017.71","article-title":"ARMC5 is not implicated in familial 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low-voltage-activated t-type calcium channels","volume":"83","year":"2003","journal-title":"Physiology Review"},{"key":"ref451","doi-asserted-by":"publisher","first-page":"2015100","DOI":"10.1210\/jc.2015-2149","article-title":"meta - analysis of somatic channel mutations in patients with an aldosterone - producing adenoma of and https org","author":"KCNJ","year":"1636","journal-title":"Journal Clinical Endocrinology Metabolism"},{"key":"ref161","doi-asserted-by":"crossref","first-page":"3187","DOI":"10.1210\/jcem.87.7.8647","article-title":"Glucocorticoid remediable aldosteronism: low morbidity and mortality in a four-generation Italian pedigree","volume":"87","year":"2002","journal-title":"Journal of Clinical Endocrinology and Metabolism"},{"key":"ref101","doi-asserted-by":"crossref","first-page":"333","DOI":"10.1016\/j.ecl.2011.01.012","article-title":"Glucocorticoid-remediable aldosteronism","volume":"40","year":"2011","journal-title":"Endocrinology and Metabolism Clinics of North America"},{"key":"ref301","doi-asserted-by":"publisher","first-page":"152","DOI":"10.1210\/jc.2013-2428","article-title":"novel mutation responsible for familial hyperaldosteronism type III of and https org","author":"KCNJ","journal-title":"Journal Clinical Endocrinology Metabolism"},{"key":"ref31","doi-asserted-by":"crossref","first-page":"797","DOI":"10.1161\/HYPERTENSIONAHA.111.175083","article-title":"Prevalence and characteristics of familial hyperaldosteronism: the PATOGEN study (Primary Aldosteronism in Torino \u2013 GENetic forms)","volume":"58","year":"2011","journal-title":"Hypertension"},{"key":"ref01","doi-asserted-by":"crossref","first-page":"151","DOI":"10.1016\/j.mce.2011.07.034","article-title":"Acute and chronic regulation of aldosterone production","volume":"350","year":"2012","journal-title":"Molecular and Cellular Endocrinology"},{"key":"ref21","article-title":"Cardiovascular events and target organ damage in primary aldosteronism compared with essential 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hyperaldosteronism","volume":"59","year":"2012","journal-title":"Hypertension"},{"key":"ref121","doi-asserted-by":"crossref","first-page":"32","DOI":"10.1038\/nsb0197-32","article-title":"The amino acid substitutions Ser288Gly and Val320Ala convert the cortisol producing enzyme, CYP11B1, into an aldosterone producing enzyme.","volume":"4","year":"1997","journal-title":"Nature Structural Biology"},{"key":"ref561","doi-asserted-by":"crossref","first-page":"4582","DOI":"10.1210\/en.2015-1466","article-title":"Pathogenesis of adrenal aldosterone-producing adenomas carrying mutations of the Na(+)\/K(+)-ATPase","volume":"156","year":"2015","journal-title":"Endocrinology"},{"key":"ref521","article-title":"Pharmacology and pathophysiology of mutated KCNJ5 found in adrenal aldosterone-producing adenomas","volume":"155","year":"2014","journal-title":"Endocrinology"},{"key":"ref321","doi-asserted-by":"crossref","first-page":"e06315","DOI":"10.7554\/eLife.06315","article-title":"Recurrent gain of 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