PassFinals
Endocrinology & Metabolic

Primary Hyperaldosteronism

Autonomous aldosterone secretion with suppressed renin, causing sodium retention, hypertension and sometimes hypokalaemia; it is a treatable cause of secondary hypertension that may be unilateral or bilateral.

In a nutshell

Autonomous aldosterone secretion suppresses renin and drives sodium retention, hypertension and sometimes hypokalaemia. Screen with paired aldosterone and renin, interpret the ARR using the local assay and medication context, then use CT/AVS to select adrenalectomy or mineralocorticoid receptor antagonist therapy.

Classic presentation

Resistant or young-onset hypertension, spontaneous or diuretic-associated hypokalaemia, an adrenal incidentaloma or a family history of early hypertension; weakness and cramps are possible but potassium may be normal.

Key points

  • The biochemical pattern is aldosterone that is inappropriately high relative to suppressed renin; interpret the ARR with the local assay and pre-test probability.
  • Normal potassium does not exclude primary aldosteronism: hypokalaemia is a severity clue, not a screening requirement.
  • Correct hypokalaemia and review interfering medicines before repeating a negative or borderline ARR; do not stop antihypertensives without specialist advice.
  • Use suppression testing selectively when intermediate-probability disease and a possible surgical pathway make confirmation useful.
  • CT shows adrenal anatomy but usually cannot establish functional lateralisation; AVS is generally needed before adrenalectomy.
  • Lateralising disease may be treated with unilateral adrenalectomy; bilateral or non-surgical disease needs an MRA, usually spironolactone, with potassium and renal monitoring.
  • An adrenal adenoma may co-secrete cortisol, so endocrine assessment for autonomous cortisol secretion matters before surgery.

First-line investigation

Paired morning aldosterone and renin with potassium, interpreted as an ARR using the local laboratory assay and medication pathway.

Management

Treat complications and refer

  • Manage severe hypertension, marked hypokalaemia, arrhythmia or neurological symptoms urgently and involve endocrine services; replace potassium when clinically indicated and monitor ECG and renal function as appropriate.2,1

Screen and interpret the ARR

  • Measure aldosterone, renin and potassium in the morning while seated; correct hypokalaemia, review interfering medicines safely and use local assay-specific cut points rather than an isolated ratio.1,2,3

Confirm only when it changes the pathway

  • Use specialist aldosterone suppression testing when intermediate-probability disease and a genuine surgical option make confirmation useful; it is not mandatory for every positive screen or when medical therapy is clearly chosen.1

Subtype before adrenalectomy

  • Use adrenal CT for anatomy and adrenal vein sampling in most surgical candidates to establish lateralisation; assess an adrenal adenoma for autonomous cortisol secretion before surgery.1

Choose targeted treatment and monitor

  • Offer specialist adrenalectomy for lateralising disease when appropriate; use lifelong MRA therapy for bilateral, unknown or non-surgical disease, then monitor blood pressure, potassium, renal function and renin during titration.1,3,2

Exam traps

  • Do not exclude primary hyperaldosteronism because potassium is normal: most patients are normokalaemic.
  • A high ARR caused by suppressed renin is not enough without considering the absolute aldosterone, assay, potassium, medicines and pre-test probability.
  • Imaging alone cannot distinguish a functioning unilateral adenoma from a non-functioning incidental nodule: AVS is usually needed before surgery.
  • NICE step-4 spironolactone for resistant hypertension is not the same as completing endocrine work-up for primary aldosteronism.

Illustrations

Renin-angiotensin-aldosterone axis in autonomous secretionDiagram contrasting normal renin-driven aldosterone release with autonomous secretion that suppresses renin through negative feedback.PassFinals · original
Distal nephron action of aldosteroneIllustration of aldosterone-driven sodium reabsorption and potassium/hydrogen excretion in the distal tubule and collecting duct.PassFinals · original
Diagnostic pathway for primary hyperaldosteronismFlowchart from aldosterone:renin ratio screening through confirmatory suppression testing to adrenal imaging and vein sampling.PassFinals · original

Key sources

  1. Endocrine Society: Primary Aldosteronism clinical practice guideline (2025) (Current specialist guideline for screening, medication-aware ARR interpretation, selective suppression testing, CT/AVS lateralisation, adrenalectomy and MRA follow-up; updated online July 2025.)
  2. NICE NG136: Hypertension in adults: diagnosis and management (Current UK recommendations for resistant hypertension, step-4 spironolactone, potassium and renal-function monitoring; guideline last updated February 2026.)
  3. BNF online: spironolactone and eplerenone (Current UK prescribing, contraindication, interaction, potassium and renal-function monitoring cross-check for mineralocorticoid receptor antagonists; consult live monographs before prescribing.)
  4. Society for Endocrinology: Keeping up with the genes in primary aldosteronism (UK specialist context on case finding, referral and the practical limitations of adrenal vein sampling; 2019 feature article, used to frame the UK versus 2025 international screening difference.)

This page is exam revision material, not medical advice, and must not be used for patient care. Always check drug doses against the BNF and current guidance. Full disclaimer.