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Treatment of primary aldosteronism

William F Young, Jr, MD, MSc
Norman M Kaplan, MD
Section Editor
André Lacroix, MD
Deputy Editor
Kathryn A Martin, MD


Primary and nonsuppressible hypersecretion of aldosterone is an increasingly recognized but still underdiagnosed cause of hypertension. The classic presenting signs of primary aldosteronism are hypertension and hypokalemia, but potassium levels are frequently normal in modern-day series of primary aldosteronism.

The overall treatment goal in patients with primary aldosteronism is to prevent the adverse outcomes associated with excess aldosterone, including hypertension, hypokalemia, renal toxicity, and cardiovascular damage. The subtype-directed treatment of primary aldosteronism will be reviewed here. The pathophysiology, clinical manifestations, and diagnosis of this disorder and other less common causes of mineralocorticoid excess are discussed separately (algorithm 1). (See "Pathophysiology and clinical features of primary aldosteronism" and "Approach to the patient with hypertension and hypokalemia" and "Familial hyperaldosteronism".)


Subtypes — Renin-independent, incompletely suppressible (primary) hypersecretion of aldosterone is an increasingly recognized, but still underdiagnosed, cause of hypertension [1]; it is estimated to be responsible for 5 to 13 percent of hypertension in humans. Many subtypes of primary aldosteronism have been described since Conn's original report of the aldosterone-producing adenoma (APA) in 1954 [2-5].

The most common types are:

Bilateral idiopathic hyperaldosteronism (or idiopathic adrenal hyperplasia [IHA], 60 to 70 percent). The underlying pathophysiology of the zona glomerulosa autonomy in patients with IHA is unknown. (See 'Idiopathic adrenal hyperplasia' below.)


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Literature review current through: Oct 2015. | This topic last updated: Oct 19, 2015.
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