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