The Curable High Blood Pressure Almost Nobody Checks For: Primary Aldosteronism | Philadelphia

TL;DR30-second take

Primary aldosteronism is a condition in which the adrenal glands make too much of the hormone aldosterone on their own, which drives up blood pressure. It is the most common identifiable cause of high blood pressure, accounting for roughly 5 to 10% of all hypertension and about a fifth of resistant cases, yet fewer than 2% of people with resistant hypertension are ever tested. It matters because the excess aldosterone harms the heart, blood vessels, and kidneys beyond what the blood pressure alone would explain, raising the risk of stroke and atrial fibrillation. It is found with a simple blood test, the aldosterone-to-renin ratio. And it is often treatable at the source: when one adrenal gland is the cause, surgery can cure or greatly improve the blood pressure, and when both are involved, a specific class of medication targets it directly. In 2025, the main guideline began recommending that essentially everyone with high blood pressure be screened at least once.

TL;DR: Primary aldosteronism is the most common identifiable cause of high blood pressure, and one of the most overlooked. In it, the adrenal glands overproduce the hormone aldosterone on their own, which makes the body hold onto sodium and water and raises blood pressure. It accounts for roughly 5 to 10% of all hypertension and about a fifth of resistant hypertension, yet fewer than 2% of people with resistant hypertension, the group most likely to have it, are ever tested. It deserves attention for a specific reason: the excess aldosterone damages the heart, arteries, and kidneys beyond what the blood pressure number alone would predict, with markedly higher rates of stroke and atrial fibrillation than ordinary high blood pressure. It is found with a simple blood test, the aldosterone-to-renin ratio, and it is often treatable at its source: a one-sided cause can be cured or greatly improved by removing that adrenal gland, and a two-sided cause is treated with a targeted medication. In 2025, the leading guideline shifted toward recommending that nearly everyone with high blood pressure be screened for it at least once.

What is primary aldosteronism?

Aldosterone is a hormone made by the adrenal glands, the two small glands that sit atop the kidneys. Its job is to manage the body's salt and water balance by telling the kidneys to hold onto sodium and water and to shed potassium. Normally its production is kept in check by a control system involving a kidney hormone called renin, which acts like a thermostat.

In primary aldosteronism, that thermostat is bypassed. One or both adrenal glands produce aldosterone autonomously, regardless of what the body needs, and the renin system is suppressed in response. The result is too much sodium and water retained, which raises blood pressure, and often, but not always, a low potassium level. That last point is a common trap: many people assume primary aldosteronism always shows up as low potassium, but most people who have it have normal potassium, so a normal level does not rule it out. It is the most common identifiable cause of high blood pressure, meaning the most common form that has a specific, findable driver rather than the catch-all of ordinary hypertension.

How common is it, and why is it missed?

More common than almost anyone treats it as, which is the heart of the problem. For decades it was considered rare, a footnote thought to cause about 1% of high blood pressure. That estimate turned out to be far too low. In an unselected primary-care population, primary aldosteronism was found in a share of hypertensive patients that rose with severity, from about 4% in mild hypertension to nearly 12% in severe hypertension.¹ The broadly accepted figure now is that it accounts for roughly 5 to 10% of all high blood pressure. Among people with resistant hypertension, the kind that stays high despite three or more medications, the share is far higher, about a fifth, with careful studies putting it around 22%.²

Set against how common it is, how rarely it is looked for is striking. In a study of more than 260,000 people with resistant hypertension, the very group most likely to have primary aldosteronism, only about 1.6% were ever tested for it.³ That gap, between how often the condition is present and how seldom it is sought, is why it is described as the curable high blood pressure almost nobody checks for. Most people with it are carrying a specific, treatable driver of their hypertension that no one has named.

Why does it matter more than the blood pressure number?

This is the part that changes how seriously to take it. Primary aldosteronism is more than another route to the same high blood pressure: the aldosterone excess itself inflicts extra damage on the cardiovascular system, above and beyond the pressure it creates.

When people with primary aldosteronism are compared with people who have ordinary high blood pressure at the same level, those with aldosterone excess have substantially higher rates of serious cardiovascular events. A large analysis found their odds of stroke were about two and a half times higher, their odds of atrial fibrillation more than three times higher, and their odds of coronary artery disease and heart failure meaningfully raised as well, all compared with matched patients whose blood pressure was just as high from ordinary causes.⁴ The excess aldosterone appears to drive inflammation and scarring in the heart, blood vessels, and kidneys directly, which is why the harm outruns the blood pressure reading. That is the strongest argument for finding it: two people can have identical numbers on the cuff, and the one whose hypertension is driven by aldosterone is on a worse path unless the aldosterone itself is addressed.

Who should be screened, and how is it found?

Until recently, screening was aimed at higher-risk groups, and that list is still a useful floor. It includes anyone with resistant hypertension, high blood pressure together with a low potassium level, high blood pressure found alongside an adrenal nodule on a scan, high blood pressure with obstructive sleep apnea, hypertension that started young or came with a stroke at a young age, and anyone with a close relative who has primary aldosteronism.⁶ If any of those describes you, screening is clearly warranted.

The direction has since widened. In 2025, the main guideline moved toward recommending that essentially everyone with high blood pressure be screened for primary aldosteronism at least once. That change reflects how common and how consequential it turns out to be.⁵ This is a conditional recommendation rather than an absolute rule, but the direction of travel is unmistakably toward more screening, not less.

The screening test itself is a blood test called the aldosterone-to-renin ratio, which measures the aldosterone level against the suppressed renin that gives the condition away. A positive screen is then confirmed with a further test, and if confirmed, imaging of the adrenal glands and sometimes a specialized procedure called adrenal vein sampling are used to work out whether one gland or both are responsible, which determines the treatment. One practical wrinkle matters here: several blood pressure medications, particularly a class called mineralocorticoid receptor antagonists, can distort the screening test, so the timing and interpretation need to be managed by a physician. That is a reason to coordinate testing carefully rather than a reason to skip it, and it is never a reason to stop or change your blood pressure medications on your own.

Can it be cured?

Often, yes, at least in the sense that matters, and this is what makes finding it so worthwhile. The treatment depends on whether the aldosterone is coming from one adrenal gland or both.

When a single gland is the source, usually a small benign growth called an aldosterone-producing adenoma, removing that one gland with surgery can cure or greatly improve the high blood pressure. The honest detail is that a full cure, meaning normal blood pressure with no medication at all afterward, happens in a minority of cases, roughly a third, while the large majority get either that or a meaningful improvement, needing fewer medications for better control, and nearly all have the underlying aldosterone abnormality corrected.⁷ So the accurate promise is cure or substantial improvement rather than a guaranteed cure for everyone.

When both glands are overproducing, surgery is not the answer, and the treatment is a medication that blocks aldosterone's effect directly, a mineralocorticoid receptor antagonist such as spironolactone or eplerenone. A newer, more selective drug in this family, finerenone, has entered the guideline's list of options, though its specific long-term role in primary aldosteronism is still being defined. The key point is that even the two-sided form has a targeted treatment aimed at the underlying problem, rather than a pile of general blood pressure drugs that never address the cause.

Guidance from the Clinic

"This is one of the clearest examples of why root-cause thinking matters. When someone's blood pressure will not come down on three medications, or came on when they were young, or comes with a low potassium, my mind goes straight to aldosterone, because it is common, it is testable, and it is treatable, and yet almost no one gets checked. What I find compelling is that the harm outruns the number: two patients with the same reading are not on the same road if one of them is making too much aldosterone. So I screen the people the guidelines flag, and increasingly, in line with where the field moved in 2025, I consider it broadly. The test is a simple blood draw, timed and read correctly. And when it is positive, we can sometimes cure the blood pressure by removing one gland, or treat it directly with the right drug. That is a much better story than adding a fourth pill and hoping."

Key Takeaways

Primary aldosteronism, in which the adrenal glands overproduce aldosterone on their own, is the most common identifiable cause of high blood pressure, behind roughly 5 to 10% of all cases and about a fifth of resistant hypertension.
It is dramatically underdiagnosed: in one large study of resistant hypertension, only about 1.6% of patients were ever tested for it.
It harms the heart, arteries, and kidneys beyond the blood pressure itself, with much higher rates of stroke and atrial fibrillation than ordinary hypertension at the same level.
It is found with a simple blood test, the aldosterone-to-renin ratio, followed by confirmatory testing and imaging; normal potassium does not rule it out, and blood pressure medications should only be adjusted for testing under a physician's direction.
Treatment targets the cause: a one-sided source can be cured or greatly improved by removing that adrenal gland, and a two-sided source is treated with an aldosterone-blocking medication. In 2025, guidance moved toward screening nearly everyone with hypertension at least once.

Hypertension Management - the broader approach to high blood pressure
Finerenone (Kerendia) - the newer aldosterone-blocking drug, and where it fits
Wearable-Detected Atrial Fibrillation - one of the rhythms aldosterone excess makes more likely
Stroke Prevention - why the stroke risk here is worth acting on
The Advanced Tests Your Doctor Isn't Ordering - where the aldosterone-to-renin ratio fits a fuller workup

Scientific References

Monticone S, Burrello J, Tizzani D, et al. "Prevalence and Clinical Manifestations of Primary Aldosteronism Encountered in Primary Care Practice." Journal of the American College of Cardiology. 2017;69(14):1811-1820.
Brown JM, Siddiqui M, Calhoun DA, et al. "The Unrecognized Prevalence of Primary Aldosteronism: A Cross-sectional Study." Annals of Internal Medicine. 2020;173(1):10-20.
Cohen JB, Cohen DL, Herman DS, et al. "Testing for Primary Aldosteronism and Mineralocorticoid Receptor Antagonist Use Among US Veterans: A Retrospective Cohort Study." Annals of Internal Medicine. 2021;174(3):289-297.
Monticone S, D'Ascenzo F, Moretti C, et al. "Cardiovascular Events and Target Organ Damage in Primary Aldosteronism Compared with Essential Hypertension: A Systematic Review and Meta-Analysis." The Lancet Diabetes & Endocrinology. 2018;6(1):41-50.
Adler GK, Stowasser M, Vaidya A, et al. "Primary Aldosteronism: An Endocrine Society Clinical Practice Guideline." Journal of Clinical Endocrinology & Metabolism. 2025;110(9):2453-2495.
Funder JW, Carey RM, Mantero F, et al. "The Management of Primary Aldosteronism: Case Detection, Diagnosis, and Treatment: An Endocrine Society Clinical Practice Guideline." Journal of Clinical Endocrinology & Metabolism. 2016;101(5):1889-1916.
Williams TA, Lenders JWM, Mulatero P, et al. "Outcomes After Adrenalectomy for Unilateral Primary Aldosteronism: An International Consensus on Outcome Measures and Analysis of Remission Rates in an International Cohort (PASO)." The Lancet Diabetes & Endocrinology. 2017;5(9):689-699.

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Frequently Asked Questions

Common Questions

It is a condition in which one or both adrenal glands, the small glands above the kidneys, make too much of the hormone aldosterone on their own. Aldosterone tells the body to hold onto sodium and water and shed potassium, so an excess raises blood pressure and can lower potassium. It is the most common identifiable cause of high blood pressure, meaning the most common form with a specific, findable driver, and it is important because it is both common and often treatable at the source.

Much more common than it was long believed to be. It accounts for roughly 5 to 10% of all high blood pressure, and about a fifth of resistant hypertension, the kind that stays high on three or more medications. Despite that, it is rarely looked for: in one large study of people with resistant hypertension, only about 1.6% were ever tested. So most people who have it are never diagnosed, which is why it is called the curable high blood pressure almost nobody checks for.

Because the excess aldosterone harms the heart, arteries, and kidneys beyond what the blood pressure alone would do. Compared with people who have the same blood pressure from ordinary causes, people with primary aldosteronism have substantially higher rates of stroke, atrial fibrillation, coronary artery disease, and heart failure. The hormone drives inflammation and scarring directly, so identical numbers on the cuff do not mean identical risk, which is the main reason finding and treating it matters.

It starts with a blood test called the aldosterone-to-renin ratio, which looks for a high aldosterone level alongside a suppressed renin level. If that screen is positive, a confirmatory test follows, and then imaging of the adrenal glands, sometimes with a specialized vein-sampling procedure, determines whether one gland or both are responsible. Some blood pressure medications can affect the screening test, so the timing needs to be coordinated with a physician; that is a reason to plan the test carefully rather than to skip it, and never a reason to stop your medications on your own.

Sometimes, and often greatly improved. If it comes from a single adrenal gland, removing that gland with surgery can cure the high blood pressure, or at least improve it enough to need fewer medications; a full medication-free cure happens in a minority, while most people get a meaningful benefit. If both glands are involved, surgery is not used, and the treatment is a medication that blocks aldosterone directly, such as spironolactone or eplerenone. Either way, the treatment targets the underlying cause rather than only lowering the number.

Deep-Dive Questions

Aldosterone does more than manage salt and water; when it is present in excess, it acts on receptors throughout the heart, blood vessels, and kidneys to promote inflammation and fibrosis, the laying down of scar tissue. In the heart, that stiffening and scarring helps explain the higher rates of atrial fibrillation and heart failure; in the blood vessels, it contributes to the stroke and coronary risk; in the kidneys, it drives damage that can worsen over time. This is why two people with the same blood pressure can face different risks: the ordinary-hypertension patient has the pressure to contend with, while the aldosterone-excess patient has the pressure plus a hormone actively injuring the same organs. It is also why simply lowering the blood pressure with general drugs is not enough in primary aldosteronism; the aldosterone itself has to be blocked or removed to stop that added damage, which is the argument for treating the cause rather than the number.

Several forces line up in the wrong direction. The old teaching that it is rare, and that it should only be suspected when potassium is low, lingered long after the evidence moved on, so many clinicians do not think of it, and those who do often wrongly rule it out because the potassium is normal. The screening test has practical wrinkles, since several common blood pressure drugs affect the result, which makes some clinicians hesitant to order it. And the treatment sometimes involves referral to specialists and procedures, which adds friction. The result is a condition that is common enough to expect in any busy practice but is tested for in a tiny fraction of the people who have it. The 2025 move toward screening all people with hypertension is, in large part, an attempt to overcome that inertia by making the test routine rather than something reserved for the classic textbook case.

It is a reasonable conversation to have, and the case is strongest if you fall into a higher-risk group: blood pressure that stays high on three or more drugs, a low potassium, an adrenal nodule found on a scan, sleep apnea, or hypertension that started young. For those groups, screening has long been recommended and is clearly worthwhile. Beyond them, the ground has shifted, and as of 2025 the guideline leans toward screening essentially everyone with hypertension at least once, so asking your physician whether an aldosterone-to-renin test makes sense for you is well founded. The right framing is a shared decision with your doctor, who can time the test around your medications and interpret it correctly, rather than either demanding it or assuming it does not apply to you.

It depends on the subtype, which is why the workup does not stop at the screening test. If confirmatory testing and imaging point to one overactive gland, the option of surgery to remove it comes onto the table, and for the right person that can be the closest thing to a cure, ending or greatly reducing the need for blood pressure drugs. If both glands are involved, the path is medical: a mineralocorticoid receptor antagonist that blocks aldosterone's effect, dosed to control blood pressure and protect the organs, often alongside attention to potassium and salt. Either way, the aim is different from ordinary hypertension care: instead of stacking general medications to push the number down, the treatment is aimed squarely at the aldosterone that is causing the problem, which tends to control the pressure better and reduce the added cardiovascular harm.

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