Hyperaldosteronism (Primary)


  • Estimates of prevalence vary, but possibly up to 10% of people with hypertension
  • It is important to differentiate between extrinsic (secondary) causes of hyperaldosteronism from primary intrinsic causes
    • Most common cause of extrinsic hyperaldosteronism is inadequate renal perfusion (usually renal artery stenosis, but other causes include diuretic therapy, cardiac failure, liver failure, nephrotic syndrome)


  • Investigation for mineralocorticoid excess should be prompted in patients
    • who are hypertensive and hypokalaemic (including those on thiazide diuretics)
    • refractory hypertension
    • family history of early onset hypertension
    • early onset hypertension

Clinical Features (hyperaldosteronism)

  • Many patients will be asymptomatic but can have features of sodium retention (e.g. oedema) and hypokalaemia (e.g. muscle weakness, polyuria)
  • Hypertension is also common
  • Headache


  • Hypokalaemic acidosis
  • Sodium
    • High in primary disease (low in secondary disease because low plasma volume stimulates anti-diuretic hormone release and high angiotensin II levels stimulate thirst)
  • RAAS measurements- Aldosterone:renin ratio (ARR)- high in primary hyperaldosteronism
    • If ARR not possible, renin measurements are also used (low in primary; high in secondary)
  • Imaging- adrenal MRI


  • Most patients with primary hyperaldosteronism have idiopathic bilateral adrenal hyperplasia
  • The remainder will have aldosterone producing tumours (APA’s; Conn’s syndrome)


  • Aldosterone producing adenomas (APAs) can be managed with surgery although may require medical treatment prior to this
    • Spironolactone is the most commonly used treatments
    • Amiloride is an alternative

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