Aldosterone Test · Blood

If your blood pressure stays stubbornly high despite medication, or if you have been told you have "resistant hypertension," there is roughly a one in five chance that an overproduction of a single adrenal hormone is the real culprit. That hormone is aldosterone. And because it is almost never measured on a routine blood panel, the problem can go undetected for years while the excess quietly damages your heart, kidneys, and blood vessels.

Aldosterone (a steroid hormone made in the outer layer of your adrenal glands) tells your kidneys to hold onto sodium and release potassium. When it runs too high for too long, the sodium retention raises blood pressure and the hormone itself triggers inflammation, scarring, and stiffening in your arteries and heart muscle. Measuring your aldosterone alongside renin (the enzyme that normally controls its release) reveals whether your body is producing aldosterone inappropriately, a pattern that standard blood pressure medications alone cannot fully correct.

What Aldosterone Does in Your Body

Aldosterone is manufactured from cholesterol by a specific enzyme called CYP11B2 (aldosterone synthase), located in a narrow band of cells at the outer edge of each adrenal gland. Under normal circumstances, the renin-angiotensin-aldosterone system, or RAAS, acts like a thermostat: when blood pressure or blood volume drops, your kidneys release renin, which eventually stimulates aldosterone production. Aldosterone then tells the kidneys to reabsorb sodium and water, restoring volume and pressure.

The problem arises when one or both adrenal glands start producing aldosterone on their own, ignoring the normal renin signal. This is called primary aldosteronism, or PA. Because renin drops in response (the thermostat tries to turn itself off, but the adrenal ignores it), measuring both aldosterone and renin together, typically as the aldosterone-to-renin ratio (ARR), is the standard way to detect this pattern.

Primary Aldosteronism: Far More Common Than Most Doctors Think

For decades, PA was considered a rare curiosity affecting perhaps 1% of people with high blood pressure. That assumption has been overturned. A study of 726 hypertensive adults found a continuum of renin-independent aldosterone production that parallels the severity of hypertension, with biochemically overt PA present in 11% to 22% of people across the blood pressure spectrum. In people with resistant hypertension (blood pressure that stays high on three or more drugs), the prevalence is even higher.

Despite this, fewer than 2% of people with resistant hypertension in a large U.S. Veterans cohort ever had their aldosterone and renin measured. When testing was performed, it led to four times more use of the targeted medications that actually address the problem and better blood pressure control over the following years. The gap between how common PA is and how rarely it is tested for remains one of the biggest missed opportunities in blood pressure management.

Heart Disease Risk

Excess aldosterone damages the cardiovascular system through mechanisms that go well beyond raising blood pressure. It promotes inflammation in blood vessel walls, accelerates plaque buildup, stiffens arteries, and drives the heart muscle to thicken and scar. These effects happen even when blood pressure looks reasonably controlled on medication.

In a population-based Canadian cohort of 2,017 adults followed for about 11 years, people with suppressed renin and a high ARR had roughly twice the risk of major cardiovascular events (heart attack, stroke, heart failure hospitalization, or cardiovascular death) compared to those with normal RAAS patterns. This held after adjusting for blood pressure and other standard risk factors, meaning the aldosterone excess was doing damage independent of the blood pressure number itself.

A large registry study comparing 602 people with PA on medication to nearly 42,000 people with ordinary high blood pressure found the PA group had about twice the rate of cardiovascular events (roughly 57 vs 27 per 1,000 person-years), about twice the rate of atrial fibrillation, and 34% higher mortality. The excess risk was concentrated in those whose renin stayed suppressed despite treatment, suggesting their aldosterone excess was not being adequately controlled.

If you have high blood pressure and your aldosterone is high with suppressed renin, the cardiovascular stakes are meaningfully higher than standard hypertension alone, and targeted treatment changes the trajectory.

Kidney Damage

Aldosterone does not just affect the kidneys indirectly through blood pressure. It directly drives inflammation and scarring in kidney tissue. A study of 1,180 people found that those with PA had more protein in their urine (a sign of kidney damage) than people with ordinary hypertension matched for blood pressure and kidney filtration rate, confirming that aldosterone itself was injuring the kidneys beyond what blood pressure alone would explain.

In people with chronic kidney disease (CKD), each doubling of serum aldosterone was associated with an 11% higher risk of kidney disease progression, with those in the highest quarter having about 45% greater risk than those in the lowest. Among PA patients treated with medication alone (rather than surgery), the rate of new CKD was about 63% higher than in matched people with ordinary hypertension, and their kidney function declined nearly twice as fast, losing about 1.6 mL/min per year compared to 0.9 mL/min per year.

Metabolic Effects and Insulin Resistance

Aldosterone impairs the way your cells respond to insulin, contributing to metabolic syndrome and type 2 diabetes risk. A large Japanese multicenter study of over 3,500 people with PA found a high prevalence of diabetes, with the risk linked in part to excess cortisol production that often accompanies aldosterone overproduction. Aldosterone also directly promotes vascular insulin resistance, which compounds the cardiovascular damage in people who are obese, have high blood pressure, or already have blood sugar problems.

Cognitive Decline and Dementia

A Korean nationwide cohort study matched 3,687 people with PA to nearly 15,000 people with ordinary hypertension and followed them for about 5 years. Those with PA on medication (rather than surgery) had a 31% higher risk of all-cause dementia and a 62% higher risk of vascular dementia (the type caused by reduced blood flow to the brain). The finding persisted after adjusting for age, income, and other health conditions. People who had surgical correction of their PA did not show this excess risk.

Reference Ranges and Screening Thresholds

Aldosterone does not have clean "optimal" or "normal" ranges the way cholesterol or blood sugar do. The number that matters most is not aldosterone alone, but the relationship between aldosterone and renin, the ARR. A high aldosterone with suppressed renin is the signature of autonomous aldosterone production, and that pattern is what drives the disease risk described above.

Screening thresholds vary by assay and lab. These ranges come from Endocrine Society guidelines and large registry studies and should be treated as orientation, not absolute cutpoints. Your lab may use different units or methods.

Assay method matters significantly. Common immunoassays can overestimate aldosterone by 58% to 86% compared to mass spectrometry, especially at lower concentrations. This means a "positive" result on one assay might be negative on another. Always compare your results within the same lab and method over time.

When Results Can Be Misleading

Aldosterone has an intra-individual coefficient of variation (how much the number naturally bounces around day to day in the same person) of about 31%, and the ARR varies by about 45%. That means a single reading can easily land on either side of a screening cutpoint purely by chance. In one study of confirmed PA patients, nearly half had at least one reading below 15 ng/dL, and 29% had at least one below 10 ng/dL, on repeat testing. A single "normal" result does not rule out the condition.

Several factors can shift your aldosterone reading enough to cause a false high or false low:

• Posture and timing: Aldosterone rises when you stand and has a circadian rhythm. Guidelines recommend drawing blood mid-morning after you have been upright for at least two hours.
• Salt intake: A high-salt diet in the days before testing can suppress aldosterone and mask PA. Very low salt intake raises it. Ideally, maintain your usual diet unless your clinician instructs otherwise.
• Potassium levels: Low potassium can blunt aldosterone secretion and produce a false-negative screening result. Potassium should be checked and corrected before formal PA testing.
• Acute stress, surgery, or illness: Psychosocial stress raises plasma aldosterone for up to three hours. Major surgery and acute illness activate the entire RAAS. Avoid testing during or shortly after these events.

Several common medications also distort aldosterone and renin measurements. Beta-blockers and central alpha-agonists (like clonidine) suppress renin more than aldosterone, artificially inflating the ARR and potentially triggering a false-positive screen. Potassium-wasting diuretics and mineralocorticoid receptor antagonists (spironolactone, eplerenone) raise both renin and aldosterone, potentially masking PA. ACE inhibitors and ARBs lower aldosterone and raise renin. Dopamine-blocking antipsychotics (sulpiride, haloperidol, chlorpromazine) can acutely raise aldosterone. If you are taking any of these, your clinician may need to adjust or substitute medications before formal PA screening.

Tracking Your Trend

Given the 31% day-to-day variability and the long list of confounders, a single aldosterone measurement is best treated as a starting signal, not a final answer. If your first ARR is elevated, a repeat draw under standardized conditions (mid-morning, seated for at least 15 minutes, usual salt intake, potassium corrected, interfering medications adjusted if possible) adds confidence. If it is borderline or low but clinical suspicion is high (resistant hypertension, low potassium, adrenal incidentaloma), repeat testing or a formal suppression test is warranted.

For people being treated for PA, serial aldosterone and renin measurements help gauge whether treatment is working. In medically treated PA, the goal is not just to lower blood pressure but to unsuppress renin, which signals that the aldosterone receptor blockade is adequate. Persistently suppressed renin on treatment is associated with ongoing cardiovascular and mortality risk. Recheck every 3 to 6 months until stable, then at least annually.

What to Do With an Abnormal Result

If your ARR comes back elevated, the next steps depend on the clinical context. A confirmatory suppression test (saline infusion or oral salt loading) helps distinguish true autonomous aldosterone production from a false alarm. If confirmed, imaging with a CT scan of the adrenal glands looks for a tumor or enlargement. Adrenal vein sampling, performed by an interventional radiologist, determines whether one or both glands are overproducing. This distinction matters because unilateral disease can be cured with surgery, while bilateral disease is managed with targeted medication.

An endocrinologist with experience in PA is the right specialist for this workup. The companion tests that add the most context are renin (essential for the ARR calculation), potassium (both to aid diagnosis and to monitor), kidney function markers like creatinine and eGFR (since aldosterone directly damages kidneys), and a basic metabolic panel. If you are ordering this test proactively because of resistant or early-onset hypertension, start with aldosterone and renin together, and bring the results to a clinician who can interpret the pattern and plan next steps.