Background
In primary hyperaldosteronism (PH), aldosterone production is increased, usually in an autonomous fashion independent of the renin aldosterone angiotensin (RAAS) system in primary aldosteronism, whereas secondary hyperaldosteronism occurs due to high renin levels.
High aldosterone levels lead to excessive sodium retention in the distal renal tubule, and concomitant urinary excretion of potassium and hydrogen ions. This leads to water retention, causing hypertension and suppression of the RAAS system, alongside hypokalaemia and metabolic alkalosis in severe cases.
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