High aldosterone levels stem from one of two broad categories: a problem within the adrenal glands themselves (primary hyperaldosteronism) or a signal from elsewhere in the body telling the adrenal glands to overproduce (secondary hyperaldosteronism). Primary aldosteronism is the most common cause of secondary hypertension, affecting an estimated 6 to 20% of people with high blood pressure. Understanding which type you’re dealing with matters because the treatments differ significantly.
How Aldosterone Works in Your Body
Aldosterone is a hormone made by your adrenal glands, two small organs that sit on top of your kidneys. Its main job is regulating blood pressure and the balance of sodium and potassium in your blood. When your body senses low blood pressure or reduced blood flow to the kidneys, it kicks off a chain reaction. Your kidneys release an enzyme called renin, which triggers the production of a protein that eventually gets converted in the lungs into a powerful signaling molecule. That molecule tells your adrenal glands to release aldosterone.
Once released, aldosterone acts on your kidneys to hold onto more sodium and water while flushing out potassium. This increases blood volume and raises blood pressure. In a healthy system, the loop is self-correcting: once blood pressure normalizes, renin drops, and aldosterone production slows down. High aldosterone becomes a problem when something breaks this feedback loop, either at the adrenal gland or upstream in the signaling chain.
Primary Causes: Problems in the Adrenal Glands
In primary aldosteronism, the adrenal glands produce too much aldosterone on their own, independent of signals from the rest of the body. Renin levels are actually suppressed in this case because the body recognizes it doesn’t need more aldosterone, but the adrenal gland ignores that signal.
The two dominant causes account for nearly all cases. A benign (noncancerous) tumor on one adrenal gland, called an aldosterone-producing adenoma, is responsible for 50 to 70% of primary aldosteronism cases. This condition was first described by Dr. Jerome Conn in 1955 and is still sometimes called Conn’s syndrome. The second most common cause is bilateral adrenal hyperplasia, where both adrenal glands become enlarged and overactive, accounting for roughly 30% of cases. A less common third cause is unilateral adrenal hyperplasia, where only one gland is enlarged without a distinct tumor.
The distinction between a single-gland tumor and both-gland enlargement is clinically important. A tumor on one gland can often be surgically removed, potentially curing the condition. Bilateral hyperplasia typically requires lifelong medication since you can’t remove both adrenal glands.
Inherited Forms
Familial hyperaldosteronism runs in families and comes in at least three recognized types. Type I is caused by an abnormal fusion of two genes on chromosome 8 that control hormone production in the adrenal gland. Type III results from a mutation in a gene called KCNJ5, which affects how potassium channels function in adrenal cells. The genetic cause of Type II remains unknown. These hereditary forms are rare but worth considering if high aldosterone shows up at a young age or in multiple family members.
Secondary Causes: Signals From Outside the Adrenals
In secondary hyperaldosteronism, the adrenal glands are functioning normally but are being told to overproduce aldosterone by excessive renin. Any condition that reduces blood flow to the kidneys can trigger this overproduction, because the kidneys interpret reduced flow as a sign of low blood volume and ramp up the hormone cascade.
Renal artery stenosis, a narrowing of the blood vessels feeding the kidneys (usually from atherosclerosis or a condition called fibromuscular dysplasia), is a classic trigger. The kidneys sense reduced flow and respond as though the body is dehydrated, stimulating aldosterone even when blood volume is actually normal or high.
Heart failure is another major driver. When the heart pumps less efficiently, less blood reaches the kidneys, and the same false alarm goes off. This applies to both left-sided heart failure and cor pulmonale, where the right side of the heart fails due to lung disease. Liver cirrhosis with fluid accumulation in the abdomen and nephrotic syndrome (a kidney condition causing protein loss) also reduce effective blood flow to the kidneys and stimulate aldosterone release.
Less common secondary causes include renin-producing tumors of the kidney, obstructive sleep apnea, pregnancy, kidney failure, and even excessive licorice consumption. Real licorice contains a compound that mimics aldosterone’s effects and can disrupt the feedback loop.
What High Aldosterone Does to Your Body
The hallmark triad of high aldosterone is high blood pressure, low potassium, and a shift in blood chemistry called metabolic alkalosis (where the blood becomes too alkaline). These three findings together are a strong signal that something is driving excess aldosterone.
The high blood pressure results from aldosterone forcing your kidneys to retain sodium and water, expanding your blood volume. The low potassium happens because as sodium gets reabsorbed, potassium gets pushed out into the urine. This potassium loss can cause muscle weakness, cramping, fatigue, heart palpitations, and in severe cases, dangerous heart rhythm changes. The metabolic alkalosis occurs because aldosterone also increases bicarbonate reabsorption in the kidneys.
Over time, persistently elevated aldosterone damages blood vessels and the heart independent of its blood pressure effects. This is why treatment often includes medications that specifically block aldosterone’s receptor, not just drugs that lower blood pressure through other mechanisms.
How High Aldosterone Is Detected
The primary screening tool is the aldosterone-to-renin ratio, or ARR. This test measures both aldosterone and renin in your blood simultaneously. If aldosterone is high and renin is low (as in primary aldosteronism), the ratio will be elevated. Current guidelines recommend a cutoff of 2.4 for people under 50 and 3.7 for those 50 and older, though optimal thresholds vary slightly by age group.
Normal aldosterone levels for adults aged 18 to 99 generally fall between 3.1 and 35.4 ng/dL in a blood test, and 3 to 25 micrograms per 24 hours in a urine collection. These ranges vary between laboratories, so your results should always be interpreted against the specific reference range provided.
Medications That Skew Test Results
Many common blood pressure medications significantly affect aldosterone and renin levels, which can make testing unreliable if you’re still taking them. ACE inhibitors and angiotensin receptor blockers both lower aldosterone and raise renin, which pushes the ratio down and can mask primary aldosteronism. Beta-blockers like atenolol do the opposite: they suppress renin more than aldosterone, artificially inflating the ratio and potentially causing a false positive. Calcium channel blockers like amlodipine tend to lower the ratio. Even some diuretics raise both aldosterone and renin.
This is why doctors often switch patients to specific “neutral” medications for several weeks before testing. The active metabolite of spironolactone (a common aldosterone-blocking drug) appears not to significantly change the ratio in studies, but most clinicians still prefer to pause it before screening.
How Diet Affects Aldosterone
Salt intake has a direct and predictable effect on aldosterone levels. In studies of healthy men, moving from a very low sodium diet to a high sodium diet progressively suppressed both renin and aldosterone. At extremely high sodium intakes, aldosterone dropped to near its minimum, though it never reached zero. Even at the highest salt loads tested, the adrenal glands continued producing an estimated 10 to 30 micrograms of aldosterone per day.
This relationship is actually used diagnostically. Salt-loading tests, where you consume a high-sodium diet or receive a saline infusion, help confirm primary aldosteronism. In a healthy person, the salt load suppresses aldosterone. In someone with an autonomous adrenal source, aldosterone stays stubbornly elevated because the gland is no longer listening to the normal feedback signals. Conversely, if you’ve been eating very little salt, your aldosterone will naturally be higher as your body tries to conserve sodium, which is a normal physiological response rather than a sign of disease.