title: Cardiovascular and renal damage in primary aldosteronism: outcomes after treatment.
abstract: Primary aldosteronism (PA) is one of the common forms of curable hypertension. Recent views have suggested that PA is far from being relatively benign, as it was previously thought, but it is associated with a variety of cardiovascular and renal sequelae that reflect the capability of inappropriately elevated aldosterone to induce tissue damage over that induced by hypertension itself. The evidence supporting these views has been obtained from experiments conducted in hypertensive animal models and studies involving patients with PA. Preclinical studies have also indicated that aldosterone causes cardiovascular and renal tissue damage only in the context of inappropriate salt status. It has been suggested that untoward effects of high-salt intake are dependent on activation of mineralocorticoid receptors (MRs) that might result from increased oxidative stress and changes in the intracellular redox potential. Unilateral adrenalectomy or treatment with MR antagonists are the current options for treating an aldosterone-producing adenoma (APA) or idiopathic adrenal hyperplasia (IHA). Treatments are effective in correcting hypertension and hypokalemia, and currently available information on their capability to prevent cardiovascular events and deterioration of renal function indicates that surgery and medical treatment are equally beneficial in the long term.
authors: Hypertension Unit, Department of Internal Medicine, University of Udine, Udine, Italy. sechi@uniud.it
authors: Leonardo A
authors: LA
authors: Sechi
authors: GianLuca
authors: G
authors: Colussi
authors: Alessandro
authors: A
authors: Di Fabio
authors: Cristiana
authors: C
authors: Catena
mesh_terms: D000315:Adrenalectomy; D000450:Aldosterone / Q000009:adverse effects; D000818:Animals; D001794:Blood Pressure / Q000187:drug effects; D002319:Cardiovascular System / Q000187:drug effects; D006801:Humans; D006929:Hyperaldosteronism / Q000150:complications* / Q000503:physiopathology / Q000628:therapy; D006973:Hypertension / Q000209:etiology; D017379:Hypertrophy, Left Ventricular / Q000209:etiology; D007668:Kidney / Q000187:drug effects / Q000503:physiopathology; D018161:Receptors, Mineralocorticoid / Q000187:drug effects; D012306:Risk
chemical_list: D018161:Receptors, Mineralocorticoid; D000450:Aldosterone