The short answer
Primary aldosteronism is a hormone condition in which one or both adrenal glands make too much aldosterone, a hormone that tells the kidneys to retain sodium and water. It can raise blood pressure and lower potassium, but many people have normal potassium. It is one of the more common treatable causes of difficult-to-control hypertension in men over 40, and it is found with blood tests for aldosterone and renin rather than imaging alone.
Imagine a man in his fifties taking three blood pressure medicines, cutting sodium, walking daily, and still seeing readings that are too high. The usual explanation is that hypertension becomes harder to control with age, and sometimes that is true. But sometimes the real problem is a hormone signal coming from two small glands above the kidneys. This article explains primary aldosteronism, why it is easy to miss, and what a careful evaluation looks like.
Key takeaways
- Primary aldosteronism is a treatable hormone cause of difficult blood pressure in some men over 40.
- The central clue is aldosterone that is inappropriately high relative to suppressed renin, not low potassium by itself.
- Screening uses aldosterone, renin, and the calculated ratio, interpreted with potassium and current medications.
- A CT scan shows structure but cannot prove a nodule is the hormone source; functional testing is essential.
- Treatment may be surgical for a confirmed one-sided source or medical with mineralocorticoid-receptor blockade for bilateral disease.
The hormone, the kidney, and the feedback loop
When the kidneys sense low blood flow, blood pressure, or sodium delivery, they release renin. Renin starts a chain that signals the adrenal glands to make aldosterone. Aldosterone tells the kidneys to retain sodium and release potassium. Water follows the sodium into the bloodstream, which helps restore volume and pressure. Once the job is done, renin falls and aldosterone settles.
Primary aldosteronism breaks that relationship. The adrenal gland keeps producing aldosterone at a level that is inappropriate for the body. The expanded blood volume suppresses renin, but aldosterone does not switch off normally. That mismatch, aldosterone high relative to a suppressed renin, is the central biochemical clue.
Why this is more than a number on the cuff
All sustained high blood pressure can damage arteries and organs. Primary aldosteronism adds a separate concern: excess aldosterone can affect the heart, blood vessels, and kidneys beyond the mechanical force of the pressure itself.
Compared with people who have ordinary primary hypertension at similar blood pressure levels, people with primary aldosteronism have higher rates of cardiovascular and kidney complications in observational research. The risks include stroke, atrial fibrillation, heart failure, coronary disease, and chronic kidney disease. That does not mean a diagnosis guarantees those outcomes; it means that calling the condition just hypertension can underestimate it.
Standard blood pressure medicines may lower the reading, but treatment that blocks aldosterone's action or removes a confirmed one-sided source addresses the hormonal mechanism directly.
The potassium myth
For decades, the teaching picture was simple: high blood pressure plus low potassium equals primary aldosteronism. Low potassium remains an important clue. Aldosterone tells the kidneys to release potassium, so severe hormone excess can push the level below the normal range. A diuretic may reveal the tendency, and unexplained weakness, cramps, palpitations, or an abnormal heart rhythm can bring it to attention.
But normal potassium does not rule the disorder out. Many affected people keep a potassium result inside the laboratory range, particularly when the disease is less severe. If screening is limited to people with low potassium, a substantial number of cases will never be tested.
There is a second twist. Low potassium can suppress aldosterone production and make a screening result look less suspicious than it should. The 2025 Endocrine Society guideline therefore says potassium should be measured alongside aldosterone and renin to help interpret the result. When potassium is low and a screen is negative, clinicians may correct the potassium and repeat the testing.
Potassium is part of the context. It is not the screening test by itself, and normal is not a clearance certificate.
Who should raise the question
The current Endocrine Society guideline conditionally suggests screening all people with hypertension. Conditionally matters. It reflects limited direct evidence about population-wide screening and recognizes that access, cost, laboratory methods, and specialist capacity vary.
In practice, the question is especially important when blood pressure remains above target on three medicines from different classes, usually including a diuretic, or when four or more medicines are needed to control it. Other strong clues include hypertension with spontaneous or diuretic-associated low potassium; an adrenal mass found on imaging; sleep apnea; hypertension beginning unusually young; a family history of early hypertension or stroke; or a close relative with primary aldosteronism.
New atrial fibrillation without the usual structural explanation can also raise suspicion, because aldosterone excess has a particularly strong association with this rhythm disorder.
A useful appointment question is: My blood pressure remains difficult to control. Could primary aldosteronism be contributing, and would screening with aldosterone and renin be appropriate for me? That is a request for evaluation, not a demand for one particular result or treatment.
The blood test that is simple but not simple to interpret
Screening usually begins with two hormone measurements: aldosterone and renin. The laboratory also calculates the aldosterone-to-renin ratio, often shortened to ARR.
The hallmark is suppressed renin combined with aldosterone that is too high for that low-renin state. A ratio can help reveal that mismatch, but the ratio is not meaningful without looking at the actual hormone values.
Timing and conditions matter. The guideline recommends morning collection with the patient seated and without deliberately restricting sodium for the preceding days. Potassium is checked at the same time.
Medication is the most important reason this is not a do-it-yourself test. Some blood pressure medicines can lower renin and make the ratio appear falsely high. Others can raise renin or alter aldosterone and make a real disorder easier to miss. Diuretics, beta blockers, ACE inhibitors, angiotensin-receptor blockers, mineralocorticoid-receptor antagonists, and several other medicines can affect interpretation in different ways.
That does not mean everyone must stop treatment. Abruptly changing blood pressure medication can be dangerous. The guideline describes both minimal-withdrawal and no-withdrawal approaches because safety and feasibility come first. A clinician may interpret results in light of the current medicines, substitute selected drugs temporarily when safe, or repeat the test under different conditions.
Laboratories also use different renin assays, aldosterone methods, and units. There is no single online cutoff that can be copied safely into every report. A positive screen is a doorway, not a final diagnosis. A negative screen can also require repetition when suspicion is high, potassium is low, or medication may have hidden the pattern.
From screening to diagnosis
After a suggestive screen, the next step depends on how convincing the biochemical pattern is and what the patient would do with the answer.
Some people undergo an aldosterone-suppression test. The idea is to challenge the system with sodium or another controlled protocol. In a normal response, aldosterone should suppress. In primary aldosteronism, it remains inappropriately active. These tests are not interchangeable household experiments. They have contraindications and require clinical supervision, especially in people with severe hypertension, heart failure, kidney disease, or low potassium.
The 2025 guideline does not require suppression testing in every circumstance. It may be unnecessary when the biochemical evidence is very strong, or when a person will be treated medically and is not pursuing surgery. In less clear cases, it can help estimate the probability that the disorder is present.
Once primary aldosteronism is established, the next question is anatomical and functional: is excess aldosterone mainly coming from one adrenal gland or from both? This is the fork that changes treatment.
Why a CT scan cannot settle the case
An adrenal CT scan can show the glands' structure. It may reveal a nodule, identify a large mass that needs a different evaluation, and help plan treatment. But a scan cannot prove that a nodule is producing aldosterone.
Nonfunctioning adrenal nodules become more common with age. A man over 40 may have a visible nodule on one side while the excess hormone comes from the other gland, or from both. Small aldosterone-producing areas may be too subtle to see.
For most people considering surgery, the Endocrine Society guideline suggests combining CT with adrenal-vein sampling. During this specialized procedure, an experienced interventional radiologist collects blood from veins draining both adrenal glands. Comparing hormone patterns can show whether production is lateralized mainly to one side.
Adrenal-vein sampling is technically demanding, invasive, and not available everywhere. It is not required for every patient. But when removal of one adrenal gland is being considered, it can prevent a decision based only on a misleading picture. The lesson is simple: a nodule is an image. Hormone production is a function. They are not automatically the same thing.
Two different treatment paths
If testing shows that aldosterone excess is coming mainly from one adrenal gland, and the person is a suitable surgical candidate who wants surgery, laparoscopic removal of that gland may be recommended. Surgery can normalize potassium and biochemical aldosterone excess. It often improves blood pressure and reduces the number of medicines. Some patients achieve normal pressure without medication, but many still need treatment because longstanding hypertension, vascular changes, genetics, weight, kidney function, and age do not disappear with the gland. The honest promise is improvement or potential remission, not a guaranteed cure.
When both adrenal glands are involved, surgery is generally not the answer. Treatment usually uses a mineralocorticoid-receptor antagonist, most commonly spironolactone or eplerenone. These medicines block aldosterone's effect at the kidney and other tissues. They require monitoring. Potassium can rise, kidney function can change, and blood pressure can fall as treatment begins. Spironolactone can cause breast tenderness, breast enlargement, reduced libido, or sexual side effects in some men because it also interacts with sex-hormone receptors. Eplerenone has fewer of those effects but may be more expensive and can require different dosing.
The goal is not merely to add another pill. It is to block the pathway that was driving the problem, monitor the response, and adjust the rest of the regimen safely. Lifestyle remains relevant. Sodium intake, body weight, physical activity, sleep apnea, alcohol, and other cardiovascular risks still influence blood pressure. Diagnosing a hormone disorder is not permission to ignore them.
What to bring to the appointment
If your blood pressure is difficult to control, begin with confirmation. Bring a home log. Confirm the cuff size and technique. Bring a complete medication and supplement list, including pain relievers, decongestants, stimulants, licorice products, and anything not prescribed.
Then ask three questions. First, does my pattern justify screening for primary aldosteronism? Second, could any of my medicines or my potassium level distort aldosterone and renin testing? Third, if the screen is positive, would the next step be repeat testing, suppression testing, medical treatment, or evaluation for a one-sided source?
Do not stop a beta blocker, diuretic, ACE inhibitor, ARB, spironolactone, eplerenone, or any other blood pressure medicine to prepare yourself for a test. The safest strategy depends on your pressure, heart, kidneys, potassium, and the clinical question. And do not assume that a normal potassium result, a normal-looking adrenal scan, or partial response to medication closes the case.
Commonly confused
“Primary aldosteronism always causes low potassium.”
Low potassium is an important clue, but many people with the condition have potassium within the normal range. Screening that waits for low potassium misses cases.
“A high aldosterone-to-renin ratio alone confirms the diagnosis.”
The ratio is a screening tool. Interpretation depends on the actual hormone values, potassium, medications, assay methods, and sometimes repeat or suppression testing.
“An adrenal nodule on CT proves the gland is overproducing aldosterone.”
Many nodules do not make excess hormone. Functional testing, and sometimes adrenal-vein sampling, is needed to connect the image to the hormone source.
Questions to raise with a healthcare professional
- Does my blood pressure pattern justify screening for primary aldosteronism?
- Could any of my current medicines or supplements affect aldosterone and renin results?
- If screening is positive, what are the next steps: repeat testing, suppression testing, medical therapy, or evaluation for a one-sided source?
- Would adrenal-vein sampling be useful before considering surgery in my case?
- How will we monitor potassium, kidney function, and blood pressure if treatment is started?
When to seek care
Worth a routine appointment
- Blood pressure that stays above target despite three or more medicines from different classes.
- Hypertension with low potassium, an adrenal nodule found incidentally, sleep apnea, atrial fibrillation, or a family history of early high blood pressure or stroke.
- A close relative diagnosed with primary aldosteronism.
Seek help without delay
- Severe headache, chest pain, shortness of breath, or neurological symptoms with very high blood pressure.
- Fainting, palpitations with dizziness, or weakness that suggests a dangerously abnormal potassium level.
References
- Endocrine Society. Primary Aldosteronism Clinical Practice Guideline
- Journal of Clinical Endocrinology and Metabolism. Primary Aldosteronism: Diagnosis and Management (McGowan et al., 2025)
- Journal of Clinical Endocrinology and Metabolism. Systematic Review Supporting the Primary Aldosteronism Guideline (Farah et al., 2025)
- Endocrine Society. Understanding Primary Aldosteronism: Patient Guide
How this article is reviewed
Aldrick articles are written from published guidance and peer-reviewed research, checked against our evidence standards and re-reviewed when guidance changes. Spotted something inaccurate or out of date? Tell us and we will correct it and update the review date.
This article is educational. It does not diagnose conditions or replace evaluation by a qualified clinician.
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