What is primary aldosteronism (Conn syndrome)?

It is a condition where one or both adrenal glands make too much aldosterone independently of the body’s normal control system. The result is high blood pressure, often with low potassium and a mild metabolic alkalosis. Conn syndrome specifically refers to the unilateral aldosterone-producing adenoma subtype.

Far more common than most people realise. Studies suggest primary aldosteronism accounts for 5 to 10 per cent of all hypertension and up to 20 per cent of resistant hypertension. It is one of the most under-diagnosed treatable causes of secondary hypertension in the UK.

Do I have to have low potassium to have it?

No. Only around half to two-thirds of patients have hypokalaemia at diagnosis. Normal potassium does not rule out primary aldosteronism, which is why screening based on hypertension pattern matters more than the potassium result alone.

What is the aldosterone/renin ratio?

It is the specialist commissioned screening blood test that compares aldosterone with plasma renin activity. A raised ratio, after appropriate medication washout, is a signal to move on to confirmatory testing rather than a diagnosis in its own right.

Why is adrenal venous sampling needed?

CT imaging can miss small adenomas and can show incidental nodules that are not the source of aldosterone. AVS measures aldosterone directly from each adrenal vein and is the gold standard for deciding whether surgery on one gland will cure the condition.

Can Conn syndrome be cured?

Yes, in many cases. When adrenal venous sampling confirms a single overactive gland, laparoscopic adrenalectomy cures the hormone excess in the majority of patients. Blood pressure often improves substantially and hypokalaemia typically resolves, though some people still need antihypertensive medication afterwards.

Health condition · Clinically reviewed

Hyperaldosteronism, Conn syndrome, and the hypertension that hides in plain sight.

Primary aldosteronism causes 5 to 10 per cent of hypertension and is heavily under-diagnosed. A specialist commissioned pathway of ARR screening, adrenal venous sampling and, where appropriate, adrenalectomy can transform outcomes.

A radiographer guides a patient onto the bed of an advanced 3 Tesla MRI scanner in a London imaging suite

Why trust this guide

01

Clinically reviewed

Written by our editorial team and reviewed by a registered UK clinician before publication.
02

Sourced from guidance

Checked against Endocrine Society, NICE and peer-reviewed sources you can see at the end.
03

Current for 2026

Reflects modern UK specialist commissioned pathways including aldosterone/renin screening, adrenal venous sampling and laparoscopic adrenalectomy.

Key facts

Primary aldosteronism at a glance.

The essentials in plain English: what it is, the subtypes and how modern UK specialist commissioned care approaches it.

What it is

Autonomous aldosterone secretion from the adrenal cortex driving hypertension, hypokalaemia and metabolic alkalosis.
How common

The most common cause of secondary hypertension, present in 5 to 10 per cent of people with hypertension and heavily under-diagnosed.
Main subtypes

Aldosterone-producing adenoma (Conn syndrome, unilateral) and bilateral idiopathic adrenal hyperplasia (IHA), plus rarer unilateral hyperplasia and familial forms.
Familial forms

FH-I (glucocorticoid-remediable), FH-II (CLCN2), FH-III (KCNJ5) and FH-IV (CACNA1H) with early-onset resistant hypertension.
Screening

Aldosterone-to-renin ratio (ARR) after medication washout, guided by specialist endocrinology.
Curable

Unilateral disease confirmed on adrenal venous sampling is often cured by laparoscopic adrenalectomy.

Why this guide matters

A treatable cause of hypertension that is routinely missed.

Primary aldosteronism is one of the most under-diagnosed conditions in adult medicine. Getting to it changes both blood pressure and long-term cardiovascular risk.

Screening is simple, if you think of it

An aldosterone/renin ratio picks up primary aldosteronism when the pattern of hypertension warrants a look.
Lateralisation decides the treatment

Adrenal venous sampling separates unilateral disease that can be cured surgically from bilateral disease treated medically.
Cardiovascular risk goes beyond blood pressure

Aldosterone excess drives stroke, atrial fibrillation and kidney damage independently of blood pressure levels, which is why targeted treatment matters.

How the diagnosis is made

From suspected hypertension to a definitive plan.

The steps a specialist endocrinologist will typically follow, in order, so you know what to expect at each stage.

Phase 1 · Assessing

Recognising the pattern and preparing for testing

Phase 2 · Confirming

Biochemistry and imaging

Phase 3 · Lateralising

Adrenal venous sampling

01

Assessing

Suspect the diagnosis

Consider primary aldosteronism in resistant hypertension, hypertension with hypokalaemia, hypertension under 40 and any adrenal incidentaloma with raised blood pressure.
02

Assessing

Baseline blood pressure and bloods

Confirm hypertension, check urea, electrolytes and kidney function. Around 30 to 50 per cent of cases have normal potassium at presentation.
03

Assessing

Medication washout

Spironolactone stopped for 6 weeks. Beta-blockers, ACE inhibitors and diuretics rationalised under specialist endocrinology guidance before screening.
04

Confirming

Aldosterone/renin ratio (ARR)

The specialist commissioned screening test. A raised ratio prompts confirmatory testing rather than immediate treatment.
05

Confirming

Confirmatory suppression testing

Saline suppression, fludrocortisone, captopril challenge or oral sodium loading, chosen and interpreted by specialist endocrinology.
06

Confirming

CT of the adrenals

Specialist commissioned imaging to look for an adenoma, bilateral hyperplasia or a rare adrenal cortical carcinoma.
07

Lateralising

Adrenal venous sampling (AVS)

The gold standard for lateralisation before surgery, performed by specialist commissioned interventional radiology at an adrenal centre.

Typical timeline: from first suspicion to a defined plan over several months, driven by the washout and confirmatory testing steps.

Symptoms

What primary aldosteronism looks like.

The pattern is stubborn hypertension, sometimes with low potassium and often without dramatic symptoms. These are the features that should prompt testing.

Resistant hypertension

Blood pressure not controlled on three or more agents including a diuretic, or requiring four or more agents at optimal doses.
Early-onset hypertension

Sustained hypertension appearing before the age of 40, especially with a family history.
Hypokalaemia

Low serum potassium, either spontaneous or worsened by thiazide or loop diuretics. Often causes cramps, weakness and polyuria.
Metabolic alkalosis

A biochemical clue on venous blood gas, often alongside hypokalaemia and hypernatraemia at the upper end of normal.
Muscle weakness and cramps

Fatigue, cramps and, when potassium falls sharply, transient paralysis. Nocturia and polyuria are common.
Adrenal incidentaloma

An adrenal mass found on imaging done for another reason, combined with hypertension, warrants a screen for primary aldosteronism.
End-organ signals

Left ventricular hypertrophy, atrial fibrillation, stroke and albuminuria at rates higher than seen in matched primary hypertension.
Red flag - hypertensive emergency

Severe uncontrolled hypertension, chest pain or neurological signs mean an urgent hospital assessment, not a routine work-up.

Treatment

How primary aldosteronism is treated in the UK.

The choice hinges on lateralisation: unilateral disease is often cured by adrenalectomy, bilateral disease is treated with a mineralocorticoid receptor antagonist.

Laparoscopic adrenalectomy

For confirmed unilateral disease on AVS. Often curative for Conn syndrome. See our guide at /treatments/adrenalectomy/ for what surgery involves.
Spironolactone

First-line medical therapy for bilateral adrenal hyperplasia or when surgery is not an option. Titrated against blood pressure and potassium.
Eplerenone

A more selective mineralocorticoid receptor antagonist for patients who cannot tolerate spironolactone side effects such as gynaecomastia.
Amiloride

A potassium-sparing option used when mineralocorticoid receptor antagonists are contraindicated or poorly tolerated.
Blood pressure optimisation

Additional agents from the standard hypertension ladder as needed. See /conditions/high-blood-pressure/ for the general framework.
Potassium correction

Oral or intravenous replacement guided by severity, with careful monitoring during medication changes.
Genetic testing

Considered in early-onset disease, strong family history or when familial hyperaldosteronism is suspected, coordinated by specialist commissioned services.
Renal denervation

A specialist option for truly resistant hypertension in selected patients. See /treatments/renal-denervation/ for how it is used.

What this guide is based on

The sources behind every claim on this page.

International specialist society guidance and UK national frameworks, current at the time of last review.

Key references

Guidelines and standards we relied on.

A quiet reminder

This guide is for information, not medical advice.

Your GP or endocrinologist knows your history and can tell you which parts apply to you. If in doubt, get seen.

Endocrine Society. Clinical Practice Guideline: Case Detection, Diagnosis, and Treatment of Patients with Primary Aldosteronism (2016).
NICE. Hypertension in adults: diagnosis and management (NG136).
British Endocrine Society position statements on adrenal disease and adrenal venous sampling.
UK adrenal centres (King’s College Hospital, Barts, Royal Free) protocols for AVS and laparoscopic adrenalectomy.

Red flags

When hyperaldosteronism needs urgent attention.

Most cases are managed on a planned outpatient pathway. These are the situations that need faster escalation or a change of approach.

Hypertensive emergency

Severe uncontrolled hypertension with headache, chest pain, breathlessness or neurological signs. Needs urgent hospital assessment.
Severe hypokalaemia

Potassium below 3.0 mmol/L, especially with ECG changes, muscle paralysis or arrhythmia. Needs monitored replacement.
Suspected adrenal carcinoma

A large, irregular or rapidly growing adrenal mass on imaging. Requires urgent specialist commissioned endocrine and surgical review.
Pregnancy

Spironolactone is avoided in pregnancy. Management changes materially and must be led by a specialist obstetric endocrinology team.
Young patients with strong family history

Consider familial hyperaldosteronism (FH-I to FH-IV). Genetic testing and first-degree relative screening may be indicated.
Sudden potassium fall on diuretic

A striking drop in potassium after starting a thiazide should always prompt consideration of primary aldosteronism.
Stroke, MI or atrial fibrillation under 50

Cardiovascular events at a young age with hypertension deserve a low threshold for secondary hypertension work-up.
Failure to reach blood pressure targets

Persistent hypertension despite adherence and three optimised agents is a classic trigger for specialist referral.
Symptomatic hypokalaemia

Cramps, weakness, palpitations or paralysis that resolve with potassium replacement should not be dismissed as isolated events.

Living with it

A long-term condition, with a clear plan.

Four things make the biggest difference day to day: consistent medication, steady monitoring, sensible lifestyle changes and family awareness.

A quiet reminder

Consistency beats intensity, every time.

Small, steady habits kept up for years do more for cardiovascular risk than short bursts of effort.

01 Adherence

Take medication consistently

Whether it is spironolactone, eplerenone or a post-surgical regime, steady daily dosing keeps aldosterone effects and blood pressure under control.
02 Monitoring

Regular blood pressure and bloods

Home blood pressure checks and periodic urea, electrolytes and kidney function are the backbone of long-term care.
03 Lifestyle

Salt, weight and alcohol

Reducing dietary salt, keeping weight in a healthy range and moderating alcohol amplify the effect of medication or surgery.
04 Family

Consider your relatives

In familial forms, first-degree relatives may benefit from screening. Ask the specialist team whether this applies to you.

Frequently asked

Everything we get asked about Conn syndrome.

Quick answers on screening, adrenal venous sampling, medical therapy and surgery.

What is primary aldosteronism (Conn syndrome)?

It is a condition where one or both adrenal glands make too much aldosterone independently of the body’s normal control system. The result is high blood pressure, often with low potassium and a mild metabolic alkalosis. Conn syndrome specifically refers to the unilateral aldosterone-producing adenoma subtype.
How common is it?

Far more common than most people realise. Studies suggest primary aldosteronism accounts for 5 to 10 per cent of all hypertension and up to 20 per cent of resistant hypertension. It is one of the most under-diagnosed treatable causes of secondary hypertension in the UK.
Do I have to have low potassium to have it?

No. Only around half to two-thirds of patients have hypokalaemia at diagnosis. Normal potassium does not rule out primary aldosteronism, which is why screening based on hypertension pattern matters more than the potassium result alone.
What is the aldosterone/renin ratio?

It is the specialist commissioned screening blood test that compares aldosterone with plasma renin activity. A raised ratio, after appropriate medication washout, is a signal to move on to confirmatory testing rather than a diagnosis in its own right.
Why is adrenal venous sampling needed?

CT imaging can miss small adenomas and can show incidental nodules that are not the source of aldosterone. AVS measures aldosterone directly from each adrenal vein and is the gold standard for deciding whether surgery on one gland will cure the condition.
Can Conn syndrome be cured?

Yes, in many cases. When adrenal venous sampling confirms a single overactive gland, laparoscopic adrenalectomy cures the hormone excess in the majority of patients. Blood pressure often improves substantially and hypokalaemia typically resolves, though some people still need antihypertensive medication afterwards.

Hyperaldosteronism, Conn syndrome, and the hypertension that hides in plain sight.

Why trust this guide

Clinically reviewed

Sourced from guidance

Current for 2026

Primary aldosteronism at a glance.

A treatable cause of hypertension that is routinely missed.

From suspected hypertension to a definitive plan.

Suspect the diagnosis

Baseline blood pressure and bloods

Medication washout

Aldosterone/renin ratio (ARR)

Confirmatory suppression testing

CT of the adrenals

Adrenal venous sampling (AVS)

What primary aldosteronism looks like.

Resistant hypertension

Early-onset hypertension

Hypokalaemia

Metabolic alkalosis

Muscle weakness and cramps

Adrenal incidentaloma

End-organ signals

Red flag - hypertensive emergency

How primary aldosteronism is treated in the UK.

Laparoscopic adrenalectomy

Spironolactone

Eplerenone

Amiloride

Blood pressure optimisation

Potassium correction

Genetic testing

Renal denervation

The sources behind every claim on this page.

When hyperaldosteronism needs urgent attention.

Hypertensive emergency

Severe hypokalaemia

Suspected adrenal carcinoma

Pregnancy

Young patients with strong family history

Sudden potassium fall on diuretic

Stroke, MI or atrial fibrillation under 50

Failure to reach blood pressure targets

Symptomatic hypokalaemia

A long-term condition, with a clear plan.

Take medication consistently

Regular blood pressure and bloods

Salt, weight and alcohol

Consider your relatives

Everything we get asked about Conn syndrome.

What is primary aldosteronism (Conn syndrome)?

How common is it?

Do I have to have low potassium to have it?

What is the aldosterone/renin ratio?

Why is adrenal venous sampling needed?

Can Conn syndrome be cured?

Keep reading.

High blood pressure

Hypertension

Endocrine hypertension

Hypokalaemia

Adrenal tumours

Adrenalectomy

Renal denervation

Private CT scan