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.
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.
Key medicines
SpironolactoneStart low and titrate under the endocrine hypertension plan to blood pressure, potassium, renal function, adverse effects and biochemical response.
EplerenoneUse a specialist-selected, often divided regimen titrated to mineralocorticoid blockade and current BNF renal, potassium and interaction advice.