Synopsis
Find autonomous aldosterone excess among people with hypertension, obtain an interpretable aldosterone-renin ratio, confirm and lateralise disease, and select surgery or mineralocorticoid blockade safely.
- Primary aldosteronism is autonomous aldosterone secretion with suppressed renin, causing sodium retention, hypertension and increased potassium and hydrogen loss; hypokalaemia is a clue but not a requirement.
- Screen particularly in resistant hypertension, spontaneous or diuretic-induced hypokalaemia, hypertension with an adrenal incidentaloma, young-onset disease, sleep apnoea or a relevant family history.
- Primary aldosteronism carries cardiovascular and renal risk beyond the measured blood pressure, so specific diagnosis and mineralocorticoid receptor treatment matter even when routine antihypertensives partly control readings.
- The aldosterone-to-renin ratio is a case-detection test, not an isolated diagnosis. Interpret the aldosterone concentration and renin suppression as well as the calculated ratio.
- Hypokalaemia can suppress aldosterone and create a false-negative screen. Correct potassium and avoid deliberate sodium restriction before testing unless the specialist protocol says otherwise.
- Spironolactone, eplerenone, amiloride, diuretics, ACE inhibitors, ARBs, beta-blockers and other agents alter renin or aldosterone. Never stop essential antihypertensives without a safe substitute plan.
- Confirmatory suppression testing is selected by endocrinology and may be unsafe in uncontrolled hypertension, heart failure or renal impairment; no single saline challenge suits every patient.
- Adrenal CT describes anatomy and excludes a large suspicious mass but cannot reliably determine which gland secretes aldosterone, because non-functioning nodules and bilateral microscopic disease are common.
- Adrenal vein sampling is the established reference for lateralising unilateral versus bilateral secretion in surgical candidates, performed in an experienced centre after biochemical confirmation.
- Unilateral disease may be treated by adrenalectomy; bilateral disease and non-surgical cases receive mineralocorticoid receptor blockade with blood pressure, potassium, renal and renin response monitoring.
Key red flags
Spontaneous or diuretic-provoked hypokalaemia, metabolic alkalosis, cramps, weakness, constipation, thirst, polyuria or arrhythmia supports mineralocorticoid excess but occurs in only a subset.
Investigation priorities
Detect autonomous aldosterone production in an appropriate case-finding population.
Management branches
Resistant or young hypertension, hypokalaemia, adrenal incidentaloma, sleep apnoea or relevant family history.
- Confirm hypertension with accurate measurement, review adherence and substances, then check potassium, renal function, sodium context and the complete antihypertensive list.
- Correct hypokalaemia and coordinate medicine adjustment with endocrinology or the laboratory, substituting safer minimally interfering agents where needed without leaving severe hypertension untreated.
- Collect aldosterone and renin according to posture and timing instructions; interpret the ratio, absolute values and interference together, repeating when sampling conditions undermine confidence.
Key medicines
SpironolactoneStart low and titrate under the endocrine hypertension plan to blood pressure, potassium, renal function, adverse effects and biochemical response.Hyperkalaemia and renal decline require early laboratory checks. Gynaecomastia, breast discomfort, sexual and menstrual effects can limit adherence; interactions with other potassium-raising medicines matter.
EplerenoneUse a specialist-selected, often divided regimen titrated to mineralocorticoid blockade and current BNF renal, potassium and interaction advice.It can still cause hyperkalaemia and kidney injury and has important CYP3A4 interactions. Shorter action and lower potency may require different frequency and cost considerations.