Primary aldosteronism (PA), a significant and curable cause of secondary hypertension, is seen in 5–10% of hypertensive patients, with its prevalence contingent upon the severity of the hypertension. The principal aetiologies of PA include bilateral idiopathic hypertrophy (BIH) and aldosterone-producing adenomas (APAs), while the less frequent causes include unilateral hyperplasia, familial hyperaldosteronism (FH) types I-IV, aldosterone-producing carcinoma, and ectopic aldosterone synthesis. This condition, characterised by excessive aldosterone secretion, leads to augmented sodium and water reabsorption alongside potassium loss, culminating in distinct clinical hallmarks: elevated aldosterone levels, suppressed renin levels, and hypertension. Notably, hypokalaemia is present in only 28% of patients with PA and is not a primary indicator. The association of PA with an escalated cardiovascular risk profile, independent of blood pressure levels, is notable. Patients with PA exhibit a heightened incidence of cardiovascular events compared to counterparts with essential hypertension, matched for age, sex, and blood pressure levels. Despite its prevalence, PA remains frequently undiagnosed, underscoring the imperative for enhanced screening protocols. The diagnostic process for PA entails a tripartite assessment: the aldosterone/renin ratio (ARR) as the initial screening tool, followed by confirmatory and subtyping tests. A positive ARR necessitates confirmatory testing to rule out false positives. Subtyping, achieved through computed tomography and adrenal vein sampling, aims to distinguish between unilateral and bilateral PA forms, guiding targeted therapeutic strategies. New radionuclide imaging may facilitate and accelerate such subtyping and localisation. For unilateral adrenal adenoma or hyperplasia, surgical intervention is optimal, whereas bilateral idiopathic hyperplasia warrants treatment with mineralocorticoid antagonists (MRAs). This review amalgamates established and emerging insights into the management of primary aldosteronism.

Aldosterone, the primary adrenal mineralocorticoid hormone, as an integral part of the renin–angiotensin–aldosterone system (RAAS), is crucial in blood pressure regulation and maintaining sodium and potassium levels. It interacts with the mineralocorticoid receptor (MR) expressed in the kidney and promotes sodium and water reabsorption, thereby increasing blood pressure. However, MRs are additionally expressed in other cells, such as cardiomyocytes, the endothelium, neurons, or brown adipose tissue cells. Therefore, aldosterone (especially aldosterone excess) may have other major impacts besides simply regulating blood pressure and circulating ion balance. Recent studies have reported a non-hypertensive impact on the cardiovascular, immune, and metabolic systems, a pro-oxidant effect, and a pro-fibrotic effect. In this review, we emphasise the non-hypertension-related effects of aldosterone, including advances in our understanding of the cellular mechanisms by which aldosterone mediates its cellular effects. We also summarise potential clinical complications related to both the hypertensive and non-hypertensive effects of aldosterone.