Hyperaldosteronism is a condition where your body produces too much aldosterone, a hormone made by the adrenal glands that controls sodium and potassium balance. The excess aldosterone causes your body to hold onto sodium and water while flushing out potassium, driving up blood pressure and disrupting normal electrolyte levels. It is far more common than once believed: among people with high blood pressure, roughly 5 to 13% have primary hyperaldosteronism, and the number climbs to about 1 in 5 among those with resistant hypertension (blood pressure that stays high despite multiple medications).
Primary vs. Secondary Hyperaldosteronism
The two forms of hyperaldosteronism have fundamentally different origins, even though the end result, too much aldosterone, is the same.
In primary hyperaldosteronism (sometimes called Conn’s syndrome), the problem starts in the adrenal glands themselves. One or both glands overproduce aldosterone on their own, without being told to by the rest of the body’s hormonal signaling system. Because the adrenals are acting independently, the kidneys respond by dialing down their production of renin, the enzyme that normally triggers aldosterone release. The hallmark of primary hyperaldosteronism is high aldosterone paired with very low renin.
Secondary hyperaldosteronism works in the opposite direction. Here, the adrenal glands are functioning normally but are being overstimulated. Reduced blood flow to the kidneys, from conditions like heart failure, liver cirrhosis, or narrowed kidney arteries, triggers the kidneys to release extra renin. That renin activates a hormonal cascade that ultimately tells the adrenal glands to pump out more aldosterone. In this form, both renin and aldosterone levels are elevated.
What Causes It
For primary hyperaldosteronism, two causes account for nearly all cases. The most common is bilateral adrenal hyperplasia, where both adrenal glands become overactive due to overgrowth of adrenal tissue. This accounts for 60 to 70% of cases, and the underlying reason for the overgrowth is still unknown. The second cause, responsible for 30 to 40% of cases, is a benign (noncancerous) tumor on one adrenal gland that produces excess aldosterone. In rare instances, the condition runs in families through inherited genetic mutations.
Secondary hyperaldosteronism is caused by whatever is reducing blood flow to the kidneys. Heart failure, severe liver disease, kidney artery stenosis, and even dehydration can set off the chain reaction. Treating the underlying condition typically resolves the excess aldosterone in these cases.
Symptoms and Warning Signs
High blood pressure is the defining feature of hyperaldosteronism, and it often resists the usual treatments. If you’re taking three or more blood pressure medications and your numbers still won’t come down, hyperaldosteronism is one of the first conditions your doctor should investigate.
Low potassium (hypokalemia) is the other classic sign, though not everyone with hyperaldosteronism develops it. When potassium drops, you may notice muscle weakness, cramping, fatigue, or excessive thirst and urination. Severe potassium depletion can cause heart rhythm irregularities and, in rare cases, temporary paralysis or inability to move. Many people with hyperaldosteronism, however, have no obvious symptoms beyond stubborn high blood pressure, which is why it often goes undiagnosed for years.
How It’s Diagnosed
Screening starts with a blood test that measures the ratio of aldosterone to renin in your blood. Current guidelines use an aldosterone-to-renin ratio as the initial screening tool, with a commonly adopted cutoff of 3.7 (ng/dL)/(mU/L). A ratio above the threshold doesn’t confirm the diagnosis on its own but flags you for further testing.
A confirmatory test is the next step. The most widely used is the salt loading test, where you receive a saline infusion over four hours while resting in a semi-reclined position. Blood pressure is checked every 30 minutes throughout. The idea is straightforward: flooding your body with salt should suppress aldosterone production in a healthy person. If aldosterone levels remain high afterward, primary hyperaldosteronism is confirmed. There are also oral salt loading and other suppression tests that work on the same principle.
Once primary hyperaldosteronism is confirmed, the critical question becomes whether one adrenal gland or both are responsible, because the answer determines treatment. Adrenal vein sampling is the gold standard for making this distinction. The procedure involves threading a catheter into the veins draining each adrenal gland and measuring aldosterone levels directly. If one side is producing far more than the other, surgery becomes an option. If both sides are overproducing, the treatment path is medication. Current guidelines recommend adrenal vein sampling for most patients before considering surgery, with limited exceptions: patients under 35 with a clear solitary tumor on imaging and classic lab findings may be able to skip this step.
Treatment for One-Sided Disease
When a single adrenal gland is the source, surgical removal of that gland (typically done laparoscopically) offers the possibility of a cure. Results are encouraging but worth understanding clearly. In a study evaluating outcomes using standardized criteria, 48% of patients achieved complete clinical success, meaning their blood pressure normalized without medication. Another 43% had partial success, with blood pressure becoming easier to manage on fewer medications. Only 9% saw no clinical improvement. Overall, 91% of patients benefited from surgery.
Recovery is relatively quick. The average hospital stay after surgery is about 2 to 3 days, and serious surgical complications occurred in only 4% of patients. Outcomes are typically evaluated at a six-month follow-up, since blood pressure can take time to fully adjust after the overactive gland is removed.
Treatment for Bilateral Disease
When both adrenal glands are involved, surgery isn’t practical, and treatment relies on medications that block aldosterone’s effects. These drugs, called mineralocorticoid receptor antagonists, prevent aldosterone from acting on the kidneys even though the hormone is still being overproduced.
Spironolactone is the most commonly used option and has been a mainstay of treatment since the 1970s. For blood pressure control, doses between 50 and 100 mg daily are typical, and taking it once a day is generally as effective as splitting the dose. When added to an existing blood pressure regimen, spironolactone can lower blood pressure by an average of 21/10 mmHg within six weeks, with the effect persisting at six months. The main drawback is side effects related to its interaction with other hormone receptors: breast tenderness or enlargement in men, menstrual irregularities in women, and reduced sex drive.
Eplerenone is a newer alternative that targets aldosterone more selectively, producing fewer of those hormonal side effects. It’s effective in doses of 50 to 200 mg daily. Either medication requires lifelong use for bilateral disease, along with regular monitoring of potassium levels to avoid them swinging too high.
Risks of Leaving It Untreated
Excess aldosterone does more damage than high blood pressure alone. Aldosterone directly injures blood vessel walls and heart tissue independent of its blood pressure effects, which is why people with hyperaldosteronism face higher cardiovascular risk than people with the same degree of high blood pressure from other causes. Untreated, the condition significantly raises the risk of heart attack, heart failure, stroke, irregular heart rhythms, and kidney failure. Research comparing surgical treatment to medication has found that surgery, when appropriate, is associated with lower all-cause mortality, fewer cardiovascular events, and a lower risk of progressive kidney disease compared to medical therapy alone. Identifying and treating hyperaldosteronism early, rather than simply treating the high blood pressure it causes, can meaningfully change long-term health outcomes.