This condition has several known causes including genetic disorders, acquired conditions, metabolic derangements, and dietary imbalances. All causes mimic the effects of elevated aldosterone without raising aldosterone levels but achieve this through varying mechanisms. Genetic forms Genetic disorders that lead to this condition include Liddle's syndrome, Apparent mineralocorticoid excess (AME), and two types of Congenital adrenal hyperplasia (CAH). * Liddle's syndrome is autosomal dominant disorder affecting epithelial sodium channels (ENaC) in the distal tubules of the kidneys. In this disorder, a gain of function mutation decreases ENaC degradation leading to increased renal absorption of sodium and water. * Apparent mineralocorticoid excess genetic forms include autosomal recessive disorders with mutations lowering the activity of the enzyme 11-beta-hydroxysteroid dehydrogenase type 2 (11-β-HSD2). These mutations limit the ability of 11-β-HSD2 to transform active cortisol to the less active cortisone. Excess cortisol is then able to bind and activate mineralocorticoid receptors due to receptor cross-reactivity leading to aldosterone-like effects. * Congenital Adrenal Hyperplasia is an autosomal recessive disorder with multiple types, two of which lead to<unk> . Deficiency of 11-beta-hydroxylase blocks the conversion of 11-deoxycorticosterone (DOC) to corticosterone leading to an excess of DOC which acts as a mineralocorticoid similar to aldosterone. Deficiency of 17-alpha-hydroxylase blocks the conversion of pregnenolone and progesterone to their 17-a-hydroxy forms leading to increased mineralocorticoid production. Acquired forms Some causes of<unk>  can be acquired throughout life with examples including adrenal tumors and Ectopic ACTH syndrome. * Adrenal tumor subtypes include adrenal adenomas that produce 11-deoxycorticosterone (DOC) leading to increased mineralocorticoid activity without elevated aldosterone. * Ectopic ACTH syndrome describes conditions leading to excess production of adrenocorticotropic hormone (ACTH) subsequently leading to mineralocorticoid production. This can arise in ectopic forms of Cushing's syndrome associated with small-cell lung cancers and other ACTH-producing tumors. The excess ACTH can saturate the 11-β-HSD2 enzyme leading to decreased conversion of cortisol to cortisone and increased mineralocorticoid effects. Metabolic and dietary forms Metabolic causes include conditions of glucocorticoid resistance and from mineralocorticoid excess which can occur following high-dose corticosteroid therapy. Dietary causes include overconsumption of licorice-containing products. Glycyrrhetinic acid in licorice inhibits the 11-β-HSD2 enzyme resulting in inappropriate stimulation of the mineralocorticoid receptor by cortisol leading to aldosterone-like effects.
Pseudohyperaldosteronism
Familial hyperaldosteronism
Primary aldosteronism
Pseudohypoaldosteronism
Hyperaldosteronism
Glucocorticoid remediable aldosteronism
Apparent mineralocorticoid excess syndrome
Hypoaldosteronism