title: Primary aldosteronism: diagnostic and treatment strategies.
abstract: Primary aldosteronism is caused by bilateral idiopathic hyperplasia in approximately two-thirds of cases and aldosterone-producing adenoma in one-third. Most patients with primary aldosteronism are normokalemic. In the clinical setting of normokalemic hypertension, patients who have resistant hypertension and hypertensive patients with a family history atypical for polygenic hypertension should be tested for primary aldosteronism. The ratio of plasma aldosterone concentration to plasma renin activity has been generally accepted as a first-line case-finding test. If a patient has an increased ratio, autonomous aldosterone production must be confirmed with an aldosterone suppression test. Once primary aldosteronism is confirmed, the subtype needs to be determined to guide treatment. The initial test in subtype evaluation is CT imaging of the adrenal glands. If surgical treatment is considered, adrenal vein sampling is the most accurate method for distinguishing between unilateral and bilateral adrenal aldosterone production. Optimal treatment for aldosterone-producing adenoma or unilateral hyperplasia is unilateral laparoscopic adrenalectomy. The idiopathic bilateral hyperplasia and glucocorticoid-remediable aldosteronism subtypes should be treated pharmacologically. All patients treated pharmacologically should receive a mineralocorticoid receptor antagonist, a drug type that has been shown to block the toxic effects of aldosterone on nonepithelial tissues.
authors.affiliation: Department of Public Health and Clinical Medicine, Umeå University Hospital, Umeå, Sweden.
authors.forename: Cecilia
authors.initials: C
authors.lastname: Mattsson
authors.forename: William F
authors.initials: WF
authors.lastname: Young
mesh_terms: D000236:Adenoma / Q000150:complications; D000310:Adrenal Gland Neoplasms / Q000150:complications; D000311:Adrenal Glands / Q000000981:diagnostic imaging; D000315:Adrenalectomy; D000450:Aldosterone / Q000097:blood / Q000652:urine; D000465:Algorithms; D000818:Animals; D000959:Antihypertensive Agents / Q000494:pharmacology; D002216:Captopril / Q000494:pharmacology; D005438:Fludrocortisone / Q000031:analogs & derivatives / Q000494:pharmacology; D006801:Humans; D006929:Hyperaldosteronism / Q000175:diagnosis* / Q000188:drug therapy / Q000503:physiopathology / Q000601:surgery / Q000628:therapy*; D007008:Hypokalemia / Q000209:etiology; D000451:Mineralocorticoid Receptor Antagonists; D012083:Renin / Q000097:blood; D014057:Tomography, X-Ray Computed
chemical_list: D000959:Antihypertensive Agents; D000451:Mineralocorticoid Receptor Antagonists; D000450:Aldosterone; D002216:Captopril; D012083:Renin; D005438:Fludrocortisone; C034635:fludrocortisone acetate