Causes
The condition is due to:
Bilateral idiopathic (micronodular) adrenal hyperplasia: 66% of cases
Adrenal adenoma (Conns disease): 33% of cases
Primary (unilateral) adrenal hyperplasia: 2% of cases
Aldosterone-producing adrenocortical carcinoma: <1% of cases
Familial Hyperaldosteronism (FH)
Glucocorticoid-remediable aldosteronism (FH type I): <1% of cases
FH type II (APA or IHA): <2% of cases
Ectopic aldosterone-producing adenoma or carcinoma: < 0.1% of cases

Genetics
40% of people with an adrenal aldosterone producing adenoma have somatic gain-of-function mutations in a single gene (KCNJ5). This gene is mutated in inherited cases of early onset primary aldosteronism and bilateral adrenal hyperplasia, albeit less frequently. These mutations tend to occur in young women with the adenoma in the cortisol secreting zona fasciculata. Adenomas without this mutation tend to occur in older men with resistant hypertension.Other genes commonly mutated in aldosterone producing adenomas are ATP1A1 ATP2B3, CACNA1D, and CTNNB1. Epidemiology
In the past, the prevalence of primary aldosteronism was considered to be less than 1% of patients with hypertension. More recent studies have reported much higher prevalence of primary aldosteronism, up-to 12.7% in primary care and to 29.8% in referral centers. Very low rates of compliance with screening guidelines lead to the underdiagnoses of primary aldosteronism. Pathophysiology
Aldosterone has effects on most or all cells of the body but, clinically, the most important actions are in the kidney, on cells of the late distal convoluted tubule and medullary collecting duct. In the principal cells aldosterone increases activity of basolateral membrane sodium-potassium ATPase and apical epithelial sodium channels, ENaC, as well as potassium channels, ROMK. These actions increase sodium reabsorption and potassium secretion.
A single adrenal gland may also be removed in cases where only one is enlarged. In cases due to enlargement of both glands, treatment is typically with medications known as aldosterone antagonists such as spironolactone or eplerenone. Other medications for high blood pressure and a low salt diet, e.g. DASH diet, may also be needed. Some people with familial hyperaldosteronism may be treated with the steroid dexamethasone.Primary aldosteronism is present in about 10% of people with high blood pressure. It occurs more often in women than men. Often, it begins in those between 30 and 50 years of age. Conns syndrome is named after Jerome W. Conn (1907–1994), an American endocrinologist who first described adenomas as a cause of the condition in 1955. Signs and symptoms
People often have few or no symptoms. They may get occasional muscular weakness, muscle spasms, tingling sensations, or excessive urination.High blood pressure, manifestations of muscle cramps (due to hyperexcitability of neurons secondary to low blood calcium), muscle weakness (due to hypoexcitability of skeletal muscles secondary to hypokalemia), and headaches (due to low blood potassium or high blood pressure) may be seen.Secondary hyperaldosteronism is often related to decreased cardiac output, which is associated with elevated renin levels.