In 1955, Dr Jerome W. Conn, the American endocrinologist, first described the condition and named it Conn's syndrome.<unk>  may be classified into five groups, include adrenal carcinoma, familial hyperaldosteronism type I and II, Idiopathic hyperaldosteronism (IH),<unk>  adrenal hyperplasia, and aldosterone producing adenoma (APA), which is either renin-responsive or renin-unresponsive. Conn's syndrome<unk>  features overproduction of aldosterone despite suppressed plasma renin activity (PRA). The resulting sodium retention produces hypertension, and elevated potassium excretion may cause hypokalemia. Patients with Conn's syndrome due to<unk>  may have an aldosterone producing adrenocortical adenoma (APA); classically referred to as Conn's syndrome, a unilateral hyperplasia, idiopathic hyperaldosteronism (IHA, also known as bilateral adrenal hyperplasia), familial forms (familial hyperaldosteronism types I, II, and III) have also been described, ectopic secretion of aldosterone. Common causes of<unk>  are aldosterone-secreting adenoma, bilateral hyperplasia of the adrenal glands, and ectopic secretion of aldosterone from ovaries and kidneys.<unk>  must be differentiated from other diseases that cause hypertension and hypokalemia, such as renal artery stenosis, cushing's syndrome, congenital adrenal hyperplasia, Liddle's syndrome, diuretic use, licorice ingestion, and renin-secreting tumors. Patients with<unk>  usually appear well. Physical examination of patients with<unk>  is usually remarkable for high blood pressure, tachycardia, and an S4 maybe heard on auscultation of the precordium suggesting left ventricular hypertrophy secondary to increased afterload due to hypertension. Laboratory findings consistent with the diagnosis of<unk>  include plasma aldosterone to renin activity ratio (PAC/PRA) > 30, serum aldosterone value > 6 ng/dl, and simultaneous plasma renin activity levels < 1.0 ng/ml/hour after fludrocortisone suppression test or a plasma aldosterone > 10 ng/dl on saline infusion test or on oral sodium loading test, the post-test 24-hour urinary aldosterone excretion < 12 μg/day and a urinary sodium excretion of more than 200 mMol/day. The adrenal venous sampling test is gold standard for subtype classification of<unk> . The optimal therapy for<unk>  depends on the etiology of hyperaldosteronism. Medical therapy is indicated for bilateral adrenal hyperplasia, and all ambiguous causes of<unk> . Surgery is the mainstay of treatment for unilateral adrenal hyperplasia, aldosterone producing adenomas (APAs), adrenal carcinoma, ectopic ACTH, renin, and deoxycorticosterone secreting tumors.
Primary hyperaldosteronism
Secondary hyperaldosteronism
Familial hypoaldosteronism
Familial hyperreninemic hypoaldosteronism type 2
Hyperaldosteronism
Hypoaldosteronism
Renal artery stenosis
Dexamethasone sensitive hypertension