Aldosterone regulation plays a crucial role in maintaining intravascular and effective circulating volume and potassium homeostasis; however, inappropriate regulation of aldosterone results in adverse cardiovascular and metabolic consequences. Hyperaldosteronism can be seen in a broad range of phenotypes. Approaching hyperaldosteronism by assessing plasma renin activity and hypertensive status is a simple method to narrow the potential etiologies. Breakthroughs in genetic and histopathological research have resulted in a major paradigm shift in understanding the causes of primary aldosteronism (PA). Germline and somatic mutations in membrane channels, such as potassium channels, that maintain the resting potential of zona glomerulosa cells have been implicated in a large subset of aldosterone producing adenomas. Approaching the diagnosis of PA with an initial screening test is recommended; an aldosterone/renin ratio (ARR)>20-30 ng/dl per ng/(ml·h) when the PRA is suppressed is highly suggestive of PA. Confirmation of autonomous aldosterone excess using recommended suppression tests should prompt imaging studies to localize the source of aldosterone excess. Adrenal venous sampling can be considered in most cases to confirm the location as unilateral or bilateral, and prevent erroneous diagnoses and treatment plans; however, some emerging data suggest that the use AVS may not influence outcomes as much as previously considered. In cases of unilateral PA, surgical treatment typically results in cure of hyperaldosteronism, and substantial improvements in blood pressure and potassium homeostasis. In cases of bilateral disease, and in unilateral disease where surgery is not preferred, medical management with mineralocorticoid receptor antagonists is usually effective.
