Autonomous production of aldosterone independent of its regulators (angiotensin II/potassium)

Aetiology

Adrenal adenoma (Conn's syndrome)

• ~30% cases
• Do not suppress ACTH - adjacent and contralateral adrenal tissue is not atrophic

Genetic features

• KCNJ5 channel is a rectifying selective channel which maintains membrane hyperpolarisation
• Mutations lead to loss of ion selectivity; Na+ entry and depolarisation and therefore increased aldosterone production

Bilateral adrenal hyperplasia

• Idiopathic
• Accounts for ~60% cases

Rare causes

• Genetic mutations - several familial forms of hyperaldosteronism recognised as well as recurrent somatic mutations observed in sporadic cases
• Unilateral hyperplasia

Pathophysiology

• Commonest secondary cause of hypertension

Cardiac actions of aldosterone

• Increased cardiac collagen
• Cytokines and ROS synthesis
• Increased sodium retention