Primary aldosteronism is a condition where one or both adrenal glands produce too much aldosterone, a hormone that controls your body’s balance of sodium and potassium. It’s far more common than doctors once believed, affecting an estimated 3% to 13% of people with high blood pressure and roughly 1 in 5 people with resistant hypertension (blood pressure that stays high despite taking three or more medications).
Because excess aldosterone causes your kidneys to hold onto sodium and flush out potassium, the result is a distinctive pattern: high blood pressure that’s difficult to control, often paired with low potassium levels. The condition is treatable, and in some cases curable with surgery, but it first has to be recognized.
How Excess Aldosterone Affects Your Body
Your adrenal glands sit on top of your kidneys and produce aldosterone in a thin outer layer called the zona glomerulosa. Normally, aldosterone production rises and falls in response to signals from your kidneys and blood volume. In primary aldosteronism, that feedback loop breaks down. The adrenal tissue keeps churning out aldosterone regardless of whether your body needs it.
The excess aldosterone tells your kidneys to reabsorb more sodium from your urine back into your bloodstream. Water follows the sodium, increasing blood volume and driving up blood pressure. At the same time, your kidneys dump more potassium into the urine to compensate, which can drop your blood potassium to abnormally low levels. This combination of sodium retention and potassium loss explains most of the symptoms people experience.
Beyond its effects on blood pressure, aldosterone directly damages the heart and blood vessels. A large genetic analysis published in the Journal of the American Heart Association found that primary aldosteronism carries a two to three times higher risk of coronary artery disease, stroke, and heart failure compared to ordinary high blood pressure at the same level. That extra cardiovascular damage comes from aldosterone itself, not just from elevated blood pressure, which is why identifying and treating the condition matters so much.
Two Main Causes
Primary aldosteronism almost always traces back to one of two problems in the adrenal glands:
- A single benign tumor (aldosterone-producing adenoma). Sometimes called Conn’s syndrome, this involves a small, noncancerous growth on one adrenal gland that pumps out aldosterone independently. It accounts for roughly half of cases.
- Bilateral adrenal hyperplasia. Both adrenal glands become overactive and enlarged, each producing too much aldosterone. This is slightly more common than a single tumor and accounts for most of the remaining cases.
At the cellular level, many adenomas harbor genetic mutations that disrupt ion channels in adrenal cells. The most common mutations affect a potassium channel, causing sodium to flood into the cell instead of potassium flowing out. That triggers a chain reaction: the cell depolarizes, calcium rushes in, and the machinery for making aldosterone ramps up. Other mutations affect sodium-potassium pumps and calcium channels, but they all converge on the same outcome, more aldosterone than the body needs.
Rare hereditary forms exist as well, where the genetic mutation is present from birth and runs in families. These account for a small fraction of cases.
Common Symptoms
Many people with primary aldosteronism don’t have dramatic symptoms. The most prominent sign is high blood pressure, often stubbornly resistant to standard medications. If your blood pressure stays elevated despite taking multiple drugs, or if you developed hypertension at a young age, primary aldosteronism is one of the conditions worth investigating.
When potassium levels drop, additional symptoms appear: muscle weakness, fatigue, headaches, and numbness or tingling. Some people notice muscle cramps or an unusual amount of urination and thirst, since potassium depletion affects the kidneys’ ability to concentrate urine. That said, many patients with primary aldosteronism have normal potassium levels, at least on routine blood tests, so the absence of low potassium doesn’t rule it out.
How It’s Diagnosed
Screening starts with a blood test that measures the ratio of aldosterone to renin (a kidney enzyme that normally stimulates aldosterone production). In primary aldosteronism, aldosterone is high while renin is suppressed, because the adrenals are acting on their own rather than responding to renin’s signal. This ratio, called the aldosterone-to-renin ratio, is the standard first step.
Getting an accurate result requires some preparation. Certain blood pressure medications, including ACE inhibitors, ARBs, and beta blockers, can throw off the numbers and typically need to be switched to alternatives like diltiazem for at least four weeks before testing. Oral contraceptives and hormone replacement therapy can also interfere. Blood is drawn in the morning after you’ve been sitting upright for at least a few minutes.
If the screening ratio is elevated, a confirmatory test follows. One common approach is an oral salt loading test: you eat an extra 10 grams of salt per day for three consecutive days, then collect a 24-hour urine sample. In a healthy person, all that extra salt would suppress aldosterone production. If your aldosterone stays high despite the salt load, the diagnosis is confirmed.
Figuring Out Which Adrenal Gland Is Responsible
Once primary aldosteronism is confirmed, the next question is whether one gland or both are overproducing. This distinction matters because a single overactive gland can be removed surgically, while bilateral disease is managed with medication.
CT scans can sometimes spot an obvious tumor, but imaging alone is unreliable. Many aldosterone-producing adenomas are too small to show up on a scan, and nonfunctioning lumps on the adrenal glands are common enough to create false leads. The gold standard for telling the two sides apart is adrenal vein sampling, a procedure where a radiologist threads a thin catheter into the veins draining each adrenal gland and measures aldosterone levels from each side directly. Both the U.S. Endocrine Society and the Japan Endocrine Society recommend this test for anyone with confirmed primary aldosteronism who is considering surgery.
There are a few exceptions. Patients younger than 40 with a clear, obvious adenoma on imaging and pronounced potassium depletion may not need adrenal vein sampling, though even in young patients bilateral disease can’t be completely excluded without it. And if someone prefers lifelong medication over surgery, the test isn’t necessary.
Treatment Options
Treatment depends on whether one or both adrenal glands are involved.
Surgery for One-Sided Disease
When a single adrenal gland is the source, surgical removal of that gland (adrenalectomy, usually done laparoscopically) is the definitive treatment. The biochemical problem, excess aldosterone and low potassium, is almost always corrected after surgery. Blood pressure improvement is universal, but complete normalization without any medication happens in about half of patients, according to a meta-analysis in BMC Endocrine Disorders. The other half still need some blood pressure medication afterward, likely because years of high aldosterone have caused lasting changes in the blood vessels or because they also have underlying essential hypertension.
Younger patients, those with a shorter history of hypertension, and those taking fewer medications before surgery tend to have the best chance of coming off blood pressure drugs entirely.
Medication for Bilateral Disease
When both adrenal glands are overactive, or when surgery isn’t an option, the treatment is medication that blocks 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, with eplerenone as an alternative that causes fewer hormonal side effects like breast tenderness in men.
Doses are adjusted based on blood pressure and potassium response. Because these drugs cause the body to retain potassium rather than excrete it, potassium levels need monitoring, especially early in treatment. Most people also need additional blood pressure medications to reach their target.
Why Early Detection Matters
Primary aldosteronism isn’t just a blood pressure problem. The excess aldosterone directly promotes scarring and thickening of the heart muscle, stiffening of blood vessels, and kidney damage, all independent of blood pressure levels. Genetic studies confirm that the condition raises the risk of heart failure by roughly 8% to 10% and stroke by 8% to 13% beyond what elevated blood pressure alone would predict. The longer it goes unrecognized, the more cumulative damage occurs.
Despite being one of the most common causes of secondary hypertension, primary aldosteronism is still underdiagnosed. Many people with resistant hypertension are never screened. If your blood pressure requires three or more medications, if you developed hypertension before age 40, or if routine blood work has ever flagged low potassium, asking about screening is a reasonable step.