Hyperaldosteronism (Primary)

Background

• 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)

Investigations

• 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

Investigations

• 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

Causes

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

Management

• 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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