Hyperaldosteronism Mechanisms and Consequences

Primary Aldosteronism

The American College of Cardiology notes that primary aldosteronism represents autonomous aldosterone production that cannot be suppressed with sodium loading, distinguishing it from physiologic secretion, and accounts for 5-10% of all hypertensive patients, rising to 20% in those with resistant hypertension 1, 3
Primary aldosteronism is the most common endocrine cause of hypertension, with aldosterone-producing adenoma being the most frequent unilateral cause, typically a solitary benign tumor that autonomously secretes aldosterone 1
The Endocrine Society recommends that glucocorticoid-remediable aldosteronism (familial hyperaldosteronism type-1) should be suspected in patients with early-onset hypertension or cerebrovascular accident at young age 3

Excessive aldosterone induces hypertension through sodium retention and suppression of plasma renin activity, with increased potassium excretion causing hypokalemia if prolonged and severe, although only 50% of patients present with hypokalemia 1, 3
The toxic tissue effects of aldosterone cause greater target organ damage than primary hypertension alone, including 3.7-fold increased heart failure, 4.2-fold increased stroke, 6.5-fold increased MI, and 12.1-fold increased atrial fibrillation 3

The American Heart Association advises that hypokalemia should not be relied on as a screening marker for primary aldosteronism—it is absent in the majority of cases 2, 3