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Treatment of primary aldosteronism

William F Young, Jr, MD, MSc
Section Editor
Lynnette K Nieman, 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 current 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 and in this algorithm (algorithm 1). The pathophysiology, clinical manifestations, and diagnosis of this disorder and other less common causes of mineralocorticoid excess are discussed separately. (See "Pathophysiology and clinical features of primary aldosteronism" and "Diagnosis of primary aldosteronism" and "Familial hyperaldosteronism".)


Subtypes of primary aldosteronism — 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 up to 10 percent of hypertension in humans [2]. Many subtypes of primary aldosteronism have been described since Conn's original report of the aldosterone-producing adenoma (APA) in 1954 [3-6].

The subtypes of primary aldosteronism include:

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: Nov 2017. | This topic last updated: Dec 13, 2017.
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