Conn’s disease, also called primary aldosteronism, is a condition where one or both adrenal glands produce too much of a hormone called aldosterone. This hormone controls sodium and potassium balance in your body, and when levels stay chronically elevated, the result is high blood pressure and low potassium. It accounts for an estimated 5% to 20% of all hypertension cases, making it far more common than most people realize.
How Aldosterone Excess Affects the Body
Your adrenal glands sit on top of your kidneys and produce aldosterone to help regulate blood pressure. Under normal conditions, aldosterone tells your kidneys to hold onto sodium and release potassium. When one or both glands overproduce this hormone, too much sodium gets reabsorbed into the bloodstream, pulling water along with it. Blood volume rises, blood pressure climbs, and potassium drops to unhealthy levels.
At the cellular level, the problem traces back to calcium signaling gone wrong. Genetic mutations in adrenal cells cause ion channels to malfunction, letting calcium flood in and switch on the gene responsible for making aldosterone. The cells essentially get stuck in “on” mode, pumping out aldosterone regardless of whether the body needs it. This process also drives abnormal cell growth, which is why many cases involve a small benign tumor on the adrenal gland.
Adenoma vs. Bilateral Hyperplasia
About 80% of Conn’s disease cases are caused by a single benign tumor, called an aldosterone-producing adenoma, on one adrenal gland. The remaining 20% come from bilateral adrenal hyperplasia, where both glands are overactive due to excessive growth of aldosterone-producing tissue. In rare instances, adrenal cancer can cause the condition, though this is uncommon. Distinguishing between a one-sided tumor and two-sided overactivity is critical because the treatment path is completely different.
Symptoms of Conn’s Disease
High blood pressure and low potassium are the hallmark features. Many people discover they have the condition only after their blood pressure proves stubbornly resistant to standard medications. The low potassium, meanwhile, produces its own set of problems:
- Muscle cramps and weakness: Potassium is essential for muscle contraction, so depleted levels cause cramping, general weakness, and in severe cases, temporary paralysis.
- Fatigue: Persistent tiredness that doesn’t improve with rest.
- Excessive thirst and frequent urination: The kidneys lose their ability to concentrate urine properly, creating a cycle of thirst and bathroom trips.
- Headaches and blurred vision: Both tied to chronically elevated blood pressure.
Some people with Conn’s disease have normal potassium levels on routine blood work, which is one reason the condition often goes undiagnosed for years. The blood pressure alone may be the only visible clue.
Cardiovascular Risks of Untreated Disease
Conn’s disease is not simply “high blood pressure with an unusual cause.” Excess aldosterone directly damages the heart and blood vessels in ways that go beyond what elevated blood pressure alone would produce. Compared to people with ordinary high blood pressure at similar levels, those with primary aldosteronism face dramatically higher risks of serious complications.
The risk of atrial fibrillation is 7 to 12 times higher than in people with standard hypertension. Stroke and transient ischemic attack rates are roughly double (10.4% vs. 4.9% in one large study). Heart failure requiring hospitalization is also significantly more common. These elevated risks underscore why identifying and treating the condition matters so much, even when blood pressure appears only moderately high.
How Conn’s Disease Is Diagnosed
Screening starts with a blood test measuring aldosterone and renin, a hormone that normally stimulates aldosterone production. In Conn’s disease, aldosterone is high while renin is suppressed, because the adrenal glands are producing aldosterone on their own without renin’s signal. The ratio of aldosterone to renin (the ARR) serves as the primary screening tool. An ARR above 20 when using standard immunoassay measurements, combined with suppressed renin and aldosterone at or above 10 ng/dL, points toward the diagnosis.
The most recent Endocrine Society guidelines suggest that all individuals with hypertension be screened using this aldosterone-to-renin ratio, not just those with low potassium. This represents a shift from earlier practice, which reserved screening for more obvious cases.
After a positive screen, determining whether the excess aldosterone comes from one gland or both is the next step. CT scans can sometimes reveal a tumor, but imaging alone is unreliable. Adrenal vein sampling, where blood is drawn directly from the veins draining each adrenal gland, remains the gold standard for pinpointing the source. The procedure is technically demanding. Success rates vary by operator, averaging around 82% but ranging from 0% to 100% depending on experience. Newer imaging techniques like rotational angiography have pushed success rates toward 100% at centers that use them. When sampling successfully identifies a one-sided source, pathology confirms the diagnosis 94% of the time.
Treatment for One-Sided Disease
When the problem is a single adenoma on one adrenal gland, surgery to remove that gland is the primary treatment. The operation is typically done laparoscopically, meaning small incisions and a relatively quick physical recovery.
Potassium and sodium levels normalize in virtually all patients within six months of surgery, and aldosterone levels return to normal as well. Blood pressure improvement is more variable. In one study tracking patients over two years, about 14% achieved complete resolution of their high blood pressure and were able to stop all medications. Another 46% experienced significant improvement, needing fewer medications at lower doses. The remaining patients continued to have persistent hypertension, though their potassium-related symptoms resolved.
Several factors predict whether blood pressure will fully normalize after surgery. Younger patients, those with a shorter history of hypertension before diagnosis, and those taking fewer blood pressure medications tend to do better. Nearly 30% of patients in long-term follow-up shifted categories over two years, some improving and others worsening, which means regular blood pressure monitoring remains important even after a successful operation.
Treatment for Two-Sided Disease
When both adrenal glands are overactive, surgery is not the answer because removing both glands would leave you unable to produce essential hormones. Instead, treatment relies on medications that block aldosterone’s effects at the receptor level.
The older and more widely used option is spironolactone, which is effective but carries a notable side effect: roughly 9% of patients develop breast tissue enlargement (gynecomastia), particularly men. It can also cause breast tenderness and menstrual irregularities. A newer alternative, eplerenone, is more selective in how it blocks aldosterone and does not cause gynecomastia. Its shorter duration of action means it often needs to be taken twice daily for optimal effect. Both medications carry a risk of raising potassium too high, which requires periodic blood work to monitor.
For most people with bilateral disease, medication is a lifelong commitment. The goal is to bring blood pressure under control, restore normal potassium levels, and reduce the excess cardiovascular damage that aldosterone causes over time.