Medicine
Diagnosis and Management of Primary Aldosteronism
Quick fact
Primary aldosteronism is the most common identifiable cause of hypertension, affecting up to 10% of all hypertensives and up to 20% of those with resistant hypertension. Yet it remains underdiagnosed, leading to excess cardiovascular events.
Why this is interesting
You treat hypertension every day, but what if the cause is a small tumor in your adrenal gland? Primary aldosteronism can be cured—if you know how to find it.
Read the full explanation
Understanding Diagnosis and Management of Primary Aldosteronism
Primary aldosteronism occurs when the adrenal glands produce too much aldosterone, a hormone that tells the kidneys to hold onto sodium and excrete potassium. Think of it as a faulty thermostat: the adrenal glands keep the 'salt valve' open even when the body already has enough. This causes the body to retain fluid, raising blood pressure and depleting potassium. The most common subtypes are a single benign adrenal adenoma (Conn's syndrome) and bilateral adrenal hyperplasia. The classic workup starts with a screening blood test measuring aldosterone and renin levels. In primary aldosteronism, aldosterone is high while renin is suppressed—a ratio that can be calculated. If the ratio is positive, a confirmatory test (such as a saline infusion test) proves that aldosterone remains inappropriately high despite salt loading. Then imaging and, crucially, adrenal venous sampling help pinpoint whether the problem is one-sided (surgically curable) or in both glands (requires lifelong medication). Management is therefore personalized: unilateral adenoma candidates undergo laparoscopic adrenalectomy, while bilateral hyperplasia is treated with mineralocorticoid receptor antagonists like spironolactone or eplerenone. Early diagnosis improves blood pressure control, cardiovascular outcomes, and quality of life.
A deeper explanation
The underlying mechanism is driven by the renin-angiotensin-aldosterone system (RAAS). Normally, renin is released by the kidney in response to low blood pressure or low sodium, triggering angiotensin II, which stimulates adrenal aldosterone secretion. In primary aldosteronism, an adrenal lesion autonomously secretes aldosterone regardless of these signals. This disrupts homeostasis: aldosterone binds to mineralocorticoid receptors in the distal nephron, increasing sodium reabsorption and potassium secretion. The retained sodium expands plasma volume, suppressing renin release—this is why the aldosterone-to-renin ratio (ARR) is such a sensitive screening test. The autonomous secretion persists, leading to hypertension and often hypokalemia. The diagnosis is critical because patients with primary aldosteronism have a higher risk of cardiovascular events, stroke, and atrial fibrillation compared to age- and blood-pressure-matched essential hypertensives—likely due to direct aldosterone-induced cardiac fibrosis and vascular damage. Therefore, once diagnosed, management must aim not just at normalizing blood pressure but also at countering the effects of aldosterone excess. Surgical removal of a unilateral adenoma often cures or dramatically improves hypertension, while medical therapy with mineralocorticoid receptor antagonists provides protection even when blood pressure is normalized. This mechanistic understanding underscores the importance of systematic screening in high-risk patients, especially those with resistant hypertension or hypokalemia.