Hyperaldosteronism: primary and secondary
- Lesion
Too much aldosterone from the adrenal causes high blood pressure and low potassium. It is a common, curable cause of hypertension.
What it is
Primary hyperaldosteronism is autonomous aldosterone secretion that suppresses renin. It is one of the commonest causes of secondary hypertension. Bilateral idiopathic hyperplasia and a unilateral aldosterone-producing adenoma (Conn syndrome) cause most cases, and the distinction matters because the adenoma can be removed. Secondary hyperaldosteronism, by contrast, is driven by high renin.
Structure
- Adenoma: usually small, solitary, bright yellow, well circumscribed; lipid-laden cells resembling fasciculata or glomerulosa.
- Unlike cortisol adenomas, the adjacent and opposite cortex is not atrophic (ACTH is normal).
- Bilateral hyperplasia: diffuse or micronodular expansion of the zona glomerulosa.
- Spironolactone bodies after treatment.
Step by step
- A mutation (often KCNJ5) depolarises glomerulosa cells.
- Calcium enters and switches on aldosterone synthase (CYP11B2) and cell proliferation.
- Aldosterone acts on the collecting duct: sodium reabsorption, potassium and hydrogen excretion.
- Volume expands and blood pressure rises; renin is suppressed.
- Potassium and hydrogen losses give hypokalaemia and metabolic alkalosis.
Clinical notes
- Screen hypertensive patients with resistant hypertension, hypokalaemia or an adrenal mass using the aldosterone-to-renin ratio.
- Adrenal vein sampling separates a unilateral adenoma from bilateral hyperplasia.
- Aldosterone excess damages heart and kidney beyond blood pressure itself.
Test yourself
Think of the answer, then tap the question to see it.
How do renin levels separate primary from secondary hyperaldosteronism?
Renin is suppressed in primary and raised in secondary hyperaldosteronism.
What are spironolactone bodies?
Eosinophilic, laminated cytoplasmic inclusions seen in adrenal cortical cells after spironolactone therapy.
What is the genetic basis of glucocorticoid-remediable aldosteronism?
A chimeric CYP11B1-CYP11B2 gene that places aldosterone synthase under the ACTH-responsive 11-beta-hydroxylase promoter.
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Educational content on the mechanisms of disease; not a diagnostic or treatment guide and no substitute for a health professional's advice. No doses are given.
Sources: Familial hyperaldosteronism (MedlinePlus, US National Library of Medicine, 2025).
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Representative model, for educational purposes only.