Hyperaldosteronism & Conn’s Syndrome
Overview
Hyperaldosteronism is a state of inappropriately high aldosterone for physiological need. Aldosterone produced in the adrenal zona glomerulosa increases renal sodium reabsorption and potassium/hydrogen secretion at the distal nephron, producing volume expansion, hypertension, hypokalaemia and metabolic alkalosis.
Primary hyperaldosteronism (Conn’s syndrome) is autonomous aldosterone production with suppressed renin. Secondary hyperaldosteronism results from elevated renin driving aldosterone release.
This section emphasises recognition, immediate emergency department (ED) priorities and when to seek specialist assessment (see NICE NG136). Detailed confirmatory testing and lateralisation are specialist responsibilities.
Pathophysiology
- Aldosterone increases sodium reabsorption and increases potassium and hydrogen secretion in the distal tubule and collecting duct.
- Primary hyperaldosteronism: aldosterone secretion independent of the renin-angiotensin system; renin is usually low.
- Secondary hyperaldosteronism: raised renin (for example, renal hypoperfusion or cardiac failure) causes raised aldosterone.
- Chronic excess leads to hypertension, renal potassium wasting (hypokalaemia), metabolic alkalosis and long‑term cardiovascular and renal damage.
Common causes
When to suspect hyperaldosteronism in the ED Consider primary hyperaldosteronism when any of the following are present:
- Hypertension with young onset (for example, under 40 years) or new hypertension without typical risk factors.