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Complications include cardiovascular disease such as stroke, myocardial infarction, kidney failure and abnormal heart rhythms. [3] [4] Primary hyperaldosteronism has a number of causes. About 33% of cases are due to an adrenal adenoma that produces aldosterone, and 66% of cases are due to an enlargement of both adrenal glands. [1]
When dysregulated, aldosterone is pathogenic and contributes to the development and progression of cardiovascular and kidney disease. [8] Aldosterone has exactly the opposite function of the atrial natriuretic hormone secreted by the heart. [7] Aldosterone is part of the renin–angiotensin–aldosterone system.
Secondary hyperaldosteronism (also hyperreninism, or hyperreninemic hyperaldosteronism) is due to overactivity of the renin–angiotensin–aldosterone system (RAAS).. The causes of secondary hyperaldosteronism are accessory renal veins, fibromuscular dysplasia, reninoma, renal tubular acidosis, nutcracker syndrome, ectopic tumors, massive ascites, left ventricular failure, and cor pulmonale.
Hyperaldosteronism (the syndrome caused by elevated aldosterone) is commonly caused by either idiopathic adrenal hyperplasia or by an adrenal adenoma. The two main resulting problems: Hypertension and edema due to excessive Na+ and water retention. Accelerated excretion of potassium ions (K+). With extreme K+ loss there is muscle weakness and ...
The most common cause of primary adrenal insufficiency (Addison's disease) overall is autoimmune adrenalitis. [2] The prevalence of Addison's disease ranges from 5 to 221 per million in different countries. [30] In children, congenital adrenal hyperplasia (CAH) is the most common cause of adrenal insufficiency, with an incidence 1 in 14,200 ...
Aldosterone's effects are on the distal convoluted tubule and collecting duct of the kidney where it causes increased reabsorption of sodium and increased excretion of both potassium (by principal cells) and hydrogen ions (by intercalated cells of the collecting duct). [6]
On one hand, mutations on the gene NR3C2 (coding the mineralocorticoid receptor) cause the synthesis of a non-functional receptor which is unable to bind aldosterone or function correctly. In the kidney, aldosterone plays an important role of regulating sodium and potassium homeostasis by its actions on distal nephron cells. [3]
The kidney is directed to excrete or retain sodium via the action of aldosterone, antidiuretic hormone (ADH, or vasopressin), atrial natriuretic peptide (ANP), and other hormones. Abnormal ranges of the fractional excretion of sodium can imply acute tubular necrosis or glomerular dysfunction.