A 47-year-old female is referred to the endocrinologist for evaluation of her chronically elevated blood pressure, hypokalemia, and hypervolemia. The patient’s hypertension has been refractory to the usual medications such as beta blockers, diuretics, and angiotensin-converting enzyme (ACE) inhibitors. After a full work up including serum and urinary electrolyte levels, aldosterone suppression test, plasma aldosterone to renin ratio, and MRI which revealed an autonomous adenoma, the endocrinologist diagnoses the patient with primary hyper-aldosteronism.

Primary hyperaldosteronism can be caused by either hyperactivity in one adrenal gland (unilateral disease) or both (bilateral disease). Unilateral disease is usually caused by an aldosterone producing adenoma (benign tumor) and less commonly by adrenal cancer or hyperplasia (when the whole gland is hyperactive). Excessive autonomous secretion of aldosterone without its principle regulator, angiotension II, causes hypokalemia and induces insulin resistance; promotes inflammation, endothelial dysfunction, and cardiovascular remodeling (increased left ventricular wall and carotid intima thickness. It also affects adipose tissue differentiation and function. Therefore, primary hyperaldosteronism can influence the features of metabolic syndrome, including hypertension, obesity, dyslipidemia, insulin resistance and hyperglycemia.