Primary aldosteronism: the hidden hormone cause of high blood pressure
Last updated September 3, 2026.
Primary aldosteronism (the Conn syndrome) is the overproduction of the aldosterone (the salt-retaining hormone) by the adrenal glands: driving the high blood pressure, often with the low potassium (the cramps, the weakness, the excessive thirst-and-urination). It is the commonest curable cause of the high blood pressure (the estimated 5-10 percent of all hypertension: the widely under-tested kind), found by the simple blood test (the aldosterone-renin ratio), and treated by the surgery (the one-gland kind: often curing the pressure) or the targeted tablets (the spironolactone-kind).
What does it look like?
The high blood pressure as the main sign (often the young-onset, the severe, or the resistant-to-three-drugs kind), frequently with no other symptoms. The low-potassium effects (when present): the muscle cramps and the weakness, the excessive thirst and the urination, the headaches, and the fatigue. The typical patient discovered: the blood pressure stubborn despite the multiple medicines, or the pressure high at the unusually young age.
Why does it happen?
The adrenal gland overproducing the aldosterone: the one-sided small benign tumor (the Conn's adenoma: the third-of-cases kind, the surgically-curable) or the both-glands overactive (the bilateral hyperplasia: the tablet-managed kind). The aldosterone tells the kidneys to hoard the salt-and-water (the pressure rising) and to dump the potassium (the levels falling). It is nobody's doing: not the diet, not the lifestyle.
How is it diagnosed and treated?
- The screening blood test: the aldosterone-renin ratio (the simple bloods: worth asking for if your pressure is resistant, young-onset, or with the low potassium or the family story), with the medication adjustments sometimes needed first (the some pressure pills distort the test).
- The confirm-and-localize: the confirmatory testing, then the CT scan and sometimes the adrenal-vein sampling (the which-side question: guiding the surgery).
- The surgery for the one-sided kind: the keyhole adrenalectomy (the tumor removed: the pressure cured-or-much-improved in most).
- The tablets for the two-sided kind: the spironolactone-or-eplerenone (the aldosterone blocked: the pressure and the potassium correcting), with the salt-intake reduced.
When does it need the prompt care?
The prompt review for: the severe-or-resistant hypertension, the very low potassium symptoms (the severe cramps, the weakness, the palpitations), and the emergency for the pressure-crisis signs (the severe headache, the chest pain, the breathlessness, the neurological symptoms). Pymander's escalation routing is built and tested specifically for this class of decision; see the safety architecture working paper.
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Common questions
Why has nobody tested me before?
The known gap: the primary aldosteronism was long taught as the rare (the estimates now run the 5-10 percent of all hypertension: the common), the testing stays underused (the guidelines name the resistant-hypertension, the young-onset, the low-potassium, and the adrenal-incidentaloma groups: you are the first two), and the medication-distortion hassle puts the busy clinics off. The asking-for-the-ratio-by-name is the reasonable, evidence-based request: the blood test is cheap, and the finding changes the treatment fundamentally.
What is the difference between the one-gland and two-gland kinds?
The fork that decides the treatment: the one-sided kind (the Conn's adenoma: the small benign tumor on the one adrenal: the keyhole removal often cures-or-transforms the pressure) versus the both-glands-overactive kind (the bilateral hyperplasia: the surgery helps nobody here: the aldosterone-blocker tablets, the spironolactone-kind, are the treatment). The sorting uses the CT scan and often the adrenal-vein sampling (the catheter measuring each side's hormone: the which-side answer), and it is worth doing properly: the wrong-side surgery helps no one.
Can I just fix it with less salt?
The salt reduction helps at the margins (the aldosterone makes you retain the salt: the less-in, the less-to-retain), and it is the sensible habit either way, but it does not switch off the hormone: the overproduced aldosterone keeps driving the pressure through the ordinary-salt diets. The mechanism-specific treatment (the surgery or the blocker) is what answers the mechanism: the salt discipline complements, never replaces.
Is the surgery a big deal?
The keyhole kind in most hands (the laparoscopic adrenalectomy: the one-night-stay typical, the recovery over the 1-2 weeks), and the outcomes for the one-sided kind are the strong kind (the pressure cured-or-substantially-improved in the majority, the potassium normalizing, the some stopping all their pressure medicines). The decision rests on the localization (the adrenal-vein sampling confirming the side), and the surgical-centers' experience matters: the worth-traveling-for procedure.
Does it explain my low potassium symptoms?
Directly: the aldosterone makes the kidneys dump the potassium (the cramps, the weakness, the thirst-and-urination, the palpitations all being the low-potassium effects), and the fix targets the mechanism (the surgery or the blocker normalizing the potassium, the supplements the stopgap). The low potassium also matters for the heart (the rhythm stability), which is part of why the sorting is the priority, not the trivia.
What happens if I leave it untested?
The compounding kind: the aldosterone-driven hypertension damages faster than the ordinary hypertension (the hormone harms the heart-and-kidneys beyond the pressure alone: the fibrosis effects documented), so the years-of-the-uncontrolled-pressure accumulate the harm the ordinary readings understate. The treated kind (the blocker or the surgery) reverses the excess risk substantially. It is not the panic item; it is the worth-the-one-blood-test item, and the test is the entire cost of the finding out.