Prevention & care

Primary aldosteronism: aldosterone and renin, hypertension screening, adrenal subtypes, treatment, and outcome limits

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Primary aldosteronism involves excess adrenal aldosterone production that can raise blood pressure and disturb potassium regulation. Aldosterone and cortisol are different hormones; this is not an interchangeable label for adrenal insufficiency or every cause of hypertension.[1]

The normal renin–angiotensin–aldosterone system regulates fluid balance

The regulating system links renin, angiotensin and aldosterone with sodium, fluid and potassium balance. In primary aldosteronism, adrenal production is relatively independent of its normal regulator.[1][2]

Normal potassium does not exclude the condition

The Society’s 2025 patient guide says many people have no specific symptoms beyond hypertension. Low potassium may cause weakness or rhythm problems, but not everyone has it. A normal potassium result therefore cannot replace appropriate aldosterone/renin assessment, and hypertension should not be judged by how someone feels.[3]

Broader screening is a conditional recommendation

The 2025 guideline suggests screening all people with hypertension. It explicitly conditions implementation on resources, expertise and health-system capacity. “Suggested for a group” does not mean everyone must arrange immediate private testing or that a positive screen already establishes the final diagnosis.[2]

Its 2016 predecessor focused on higher-risk hypertension patterns, low potassium, adrenal incidentalomas, sleep apnea and relevant family history. An older summary of those criteria may explain historical practice but should not be presented as the complete July 2025 recommendation.[4]

The investigations answer different questions

The investigations answer different questions
Stage	Purpose
Screening	Measure aldosterone and renin to identify a suspicious pattern.[3]
Further assessment	Interpret the screen and decide whether additional confirmation is useful.[3]
Subtype assessment	Determine whether one adrenal or both contribute.[4]
Follow-up	Check hormonal response and blood-pressure response separately.[7][8]

The ratio depends on its components and testing context

The 2025 guideline uses aldosterone, suppressed renin and their ratio together. Assays, units, medicines, potassium and kidney disease affect interpretation. It allows clinically chosen medication-management strategies. Do not stop blood-pressure medicines or change salt intake independently to reproduce a testing protocol.[2]

A visible adrenal nodule does not alone select an operation

The 2016 guideline distinguishes CT anatomy from adrenal venous sampling for identifying unilateral or bilateral production when surgery is desired and feasible. Sampling is a specialist procedure. A growth on a scan and a demonstrated hormone source answer different questions; proceeding directly from a picture to removal can miss that distinction.[4]

Blocking aldosterone action and removing a source have different roles

The patient guide describes mineralocorticoid receptor antagonists, including spironolactone and eplerenone, as medicines that block aldosterone effects. Surgery can help selected people with a demonstrated source in one adrenal. These are disease-specific options, not a guarantee that every person can stop all blood-pressure treatment afterward.[3]

Side effects and monitoring belong in the comparison

The Society’s 2025 decision aid considers side effects, monitoring, pregnancy and cost during a clinical encounter. It lists breast or sexual/reproductive effects for spironolactone and electrolyte concerns for both options. The aid supports a clinician discussion; it does not supply a universally suitable self-selected medicine.[5]

The guideline calls for monitoring blood pressure, potassium, kidney function and renin. Its renin-directed intensification suggestion concerns uncontrolled hypertension with suppressed renin. It explicitly leaves uncertainty when blood pressure is already controlled; “maximize renin for everyone” overstates the recommendation.[2]

SPARTACUS compared diagnostic strategies using a one-year outcome

SPARTACUS randomized 200 people to CT-guided or adrenal-vein-sampling-guided management; 184 completed follow-up. Its primary endpoint was antihypertensive treatment intensity needed for target blood pressure after one year. Median defined daily drug doses were similar, with no statistically significant difference. This is a management-strategy trial, not proof that the tests identify identical glands.[6]

Surgical biochemical resolution was a secondary outcome: about 80% with CT-guided and 89% with sampling-guided adrenalectomy, also not statistically significant. The Netherlands public research organization and Warsaw cardiology institute funded the study. One nonsignificant comparison does not prove equivalence for every subgroup or long-term complication.[6]

Surgical biochemical success is not the same as medication-free blood pressure

PASO developed consensus outcome criteria and analyzed a selected international surgical cohort. Among 705 people with unilateral disease, 37% had complete clinical success and another 47% partial success; 94% of 699 with biochemical data had complete biochemical success. Follow-up classification therefore separates hormones, potassium, blood pressure and medication use.[7]

These were referral-center patients selected for unilateral adrenalectomy, not a randomized comparison with medical care. Outcomes varied between centers, and the cohort cannot supply a personal cure probability. Removing excess aldosterone can be successful while other contributors to hypertension remain.[7]

A newer medical-treatment cohort also distinguishes outcomes

The 2025 PAMO project combined expert consensus with 6–12-month data from 1,258 medically treated patients at 28 centers. Among those with available data, 52.9% had complete biochemical response and 18.3% complete clinical response. The denominators differed: 1,057 biochemical and 1,248 clinical assessments.[8]

The study reports no project funding, with individual investigators’ grants disclosed. It standardizes response categories; it did not randomize surgery versus medicines or prove one dose appropriate for everyone. Percentages from a treated cohort should not be presented as a head-to-head treatment ranking.[8]

Evidence & uncertainty

Screening guidance is conditional. Biochemical and clinical responses differ, and complete comparative appraisal remains unfinished.[2][7][8]

Selected-source overview · Independent review pending

Published questions

Does normal potassium rule out primary aldosteronism?

Selected-source overview · Independent review pending. Read the evidence context.

Many affected people do not have low potassium.[3]

Evidence behind this answer

Understanding Primary Aldosteronism: A Guide for Patients with High Blood Pressure
professional association explanation · 2025
Selected relevant original official page passages inspected · 2025, pages 1–3: symptom-poor hypertension, normal potassium, screening and treatment choices