Primary hyperaldosteronism is a condition where one or both adrenal glands produce too much aldosterone, a hormone that regulates blood pressure and the balance of sodium and potassium in your body. It’s far more common than doctors once thought, affecting roughly 5 to 10 percent of people with high blood pressure and approximately 1 in 5 people with resistant hypertension (blood pressure that stays high despite three or more medications). Because the only sign for many people is stubborn high blood pressure, it often goes undiagnosed for years.
How Excess Aldosterone Affects Your Body
Aldosterone acts on the kidneys, specifically on cells in the final stretch of the kidney’s filtering system. It tells those cells to pull sodium back into the bloodstream and push potassium out into the urine. Water follows the sodium, which increases blood volume and raises blood pressure. In a healthy system, this process is tightly regulated: when blood pressure rises or sodium levels are adequate, your body dials aldosterone production back down.
In primary hyperaldosteronism, that feedback loop is broken. The adrenal glands keep pumping out aldosterone regardless of whether the body needs it. The result is a persistent cycle of sodium retention, water retention, and elevated blood pressure. At the same time, potassium is continuously flushed out through the kidneys, which can drive levels low enough to cause symptoms throughout the body.
What Causes It
Two conditions account for the vast majority of cases. The most common is an aldosterone-producing adenoma, a small benign tumor on one adrenal gland, which is responsible for roughly 50 to 70 percent of diagnoses. The second is bilateral adrenal hyperplasia, where both adrenal glands become overactive, accounting for about 30 percent of cases. A less common third cause is unilateral adrenal hyperplasia, where only one gland is enlarged but without a distinct tumor. Rare familial forms also exist, typically diagnosed in younger patients with a strong family history of early-onset hypertension.
Distinguishing between a single-gland and a two-gland problem is critical because it determines whether surgery is an option. This distinction is called “subtyping,” and it’s a separate step after the initial diagnosis is confirmed.
Symptoms and Warning Signs
The classic textbook picture pairs high blood pressure with low potassium, but that combination is actually the exception. Fewer than 30 percent of people with confirmed primary hyperaldosteronism have significantly low potassium levels. Most present with high blood pressure alone, which is why the condition flies under the radar so often.
When potassium does drop, the symptoms can be wide-ranging: muscle weakness, fatigue, cramping, heart palpitations, and excessive thirst or urination. Some people notice they wake up multiple times at night to urinate. In more severe cases, low potassium can slow the gut, causing bloating or constipation. Headaches are also commonly reported. The tricky part is that none of these symptoms point exclusively to primary hyperaldosteronism, so the diagnosis almost always starts with a blood test rather than a symptom checklist.
How It’s Diagnosed
Screening begins with a blood test that measures the ratio of aldosterone to renin, two hormones that normally work in tandem. In primary hyperaldosteronism, aldosterone is high while renin is suppressed, producing an elevated aldosterone-to-renin ratio (ARR). Current guidelines recommend an ARR cutoff of 2.4 for people under 50 and 3.7 for those 50 and older, though the exact threshold can vary depending on the lab’s measurement units.
A positive screening result doesn’t confirm the diagnosis on its own. A confirmatory test is needed to prove that aldosterone production is truly autonomous. The most common approach is a saline infusion test, where a large volume of salt water is given intravenously over four hours. In a healthy person, the salt load would suppress aldosterone. If aldosterone remains elevated after the infusion, the diagnosis is confirmed. An alternative is the oral salt loading test, which involves eating a high-sodium diet for several days and then measuring aldosterone in a 24-hour urine collection.
Identifying the Source
Once the diagnosis is confirmed, the next step is figuring out whether one gland or both are responsible. A CT scan of the adrenal glands can sometimes reveal a clear adenoma, but imaging alone can be misleading. Small tumors can be missed, and non-functioning lumps on the adrenal glands are surprisingly common, especially with age.
Adrenal vein sampling (AVS) is considered the gold standard for subtyping. During this procedure, blood is drawn directly from the veins draining each adrenal gland so aldosterone output from each side can be compared. The Endocrine Society suggests that AVS may be skipped in patients 35 or younger who have a clear solitary adrenal lesion on imaging, spontaneous low potassium, and markedly elevated aldosterone. In these carefully selected younger patients, imaging alone predicts one-sided disease with high accuracy.
Cardiovascular Risks Beyond Blood Pressure
Primary hyperaldosteronism is not simply another form of high blood pressure. Excess aldosterone directly damages the heart and blood vessels in ways that go beyond what elevated blood pressure alone would cause. People with this condition face a 3.5-fold higher risk of developing atrial fibrillation compared to those with ordinary high blood pressure, even when blood pressure levels are similar. That increased risk translates to a greater chance of stroke and other cardiovascular events.
Aldosterone promotes inflammation and scarring (fibrosis) in heart muscle, blood vessel walls, and kidney tissue. This means that even if blood pressure numbers look acceptable on paper, the underlying organ damage can be progressing. Identifying and treating the condition early reduces these risks significantly.
Treatment Options
Treatment depends entirely on whether the excess aldosterone comes from one gland or both.
For single-gland disease caused by an adenoma, surgical removal of the affected adrenal gland is the preferred treatment. Compared to medication alone, surgery lowers systolic blood pressure by an average of nearly 9 points more, raises potassium levels more effectively, and reduces the long-term risk of cardiovascular events by about 37 percent. Many patients are able to reduce or stop their blood pressure medications after surgery, though complete cure of hypertension depends on how long the condition has been present and whether other factors are contributing.
For bilateral hyperplasia, or for patients who cannot or prefer not to have surgery, long-term medication is the standard approach. Treatment typically starts with a mineralocorticoid receptor antagonist (MRA), a type of drug that blocks aldosterone’s effects on the kidneys. Starting doses are usually low, with gradual increases over weeks to months. Most people reach an effective dose range that successfully normalizes potassium and improves blood pressure control. The main side effects to watch for relate to potassium rising too high once aldosterone is blocked, so regular blood monitoring is part of ongoing care. One commonly used MRA can also cause breast tenderness or enlargement in men, in which case an alternative MRA with fewer hormonal side effects may be substituted.
The goal of medical treatment is not just lower blood pressure readings. Clinicians now aim to fully suppress the harmful effects of excess aldosterone on organs, which is monitored in part by checking whether renin levels return to normal. Achieving this level of blockade typically requires doses in a moderate range that may be higher than what’s needed for blood pressure control alone.