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Hypoaldosteronism can be due to [[adrenal insufficiency]], [[enzyme]] deficiency ([[aldosterone synthase]], [[21-hydroxylase deficiency|21 hydroxylase]], and [[11Beta Hydroxysteroid dehydrogenase|11B hydroxylase]]), renal disorders ([[chronic renal failure]] and [[diabetic nephropathy]]) and [[drugs]] inhibiting [[aldosterone]] effect ([[Non-steroidal anti-inflammatory drug|NSAID]], [[spironolactone]], and [[triamterene]]).
Hypoaldosteronism can be due to [[adrenal insufficiency]], [[enzyme]] deficiency ([[aldosterone synthase]], [[21-hydroxylase deficiency|21 hydroxylase]], and [[11Beta Hydroxysteroid dehydrogenase|11B hydroxylase]]), renal disorders ([[chronic renal failure]] and [[diabetic nephropathy]]) and [[drugs]] inhibiting [[aldosterone]] effect ([[Non-steroidal anti-inflammatory drug|NSAID]], [[spironolactone]], and [[triamterene]]).
Aldosterone Deficiency:
Hyporeninemic hypoaldosteronism - Commonly seen in patients with renal insufficiency (diabetic kidney disease, chronic tubulointerstitial disease, or glomerulonephritis) and those that take certain medications (non-steroidal anti-inflammatory drugs, calcineurin inhibitors).[1]
Angiotensin inhibitors - angiotensin-converting enzyme (ACE) inhibitors, angiotensin II receptor blockers (ARBs), direct renin inhibitors
Heparin therapy (including low molecular weight heparin) - Heparin has a direct toxic effect on the adrenal zona glomerulosa cells which leads to a reduction in plasma aldosterone concentration.[9]
Primary adrenal insufficiency (Addison’s disease) - Associated with the lack of cortisol and aldosterone. This can result from autoimmune adrenalitis, infectious adrenalitis, and other disorders.[14]
Critical illness - There is decreased adrenal production of aldosterone and stress-induced hypersecretion of ACTH which can diminish aldosterone synthesis by diverting substrate to the production of cortisol.
Congenital isolated hypoaldosteronism - Deficiency of enzymes required for aldosterone synthesis.[14]
Pseudohypoaldosteronism type 2 (Gordon’s syndrome or familial hyperkalemic hypertension) - Abnormalities in WNK kinases in the distal nephron increase chloride reabsorption leading to reduced renal potassium secretion. Characterized by hypertension, hyperkalemia, metabolic acidosis, normal renal function, and low or low-normal plasma renin activity and aldosterone concentrations.[14][2]
Aldosterone Resistance:
Inhibitors of the epithelial sodium channel - Most commonly associated with the administation of potassium-sparing diuretics (spironolactone, eplerenone, amiloride) and certain antibiotics (trimethoprim, pentamidine).
Pseudohypoaldosteronism type 1 - Characterized by marked elevations of plasma aldosterone levels. There is an autosomal recessive form, and an autosomal dominant or sporadic form. The autosomal dominant form tends to be associated with milder symptoms

Revision as of 19:05, 18 August 2017

Hypoaldosteronism can be due to adrenal insufficiency, enzyme deficiency (aldosterone synthase, 21 hydroxylase, and 11B hydroxylase), renal disorders (chronic renal failure and diabetic nephropathy) and drugs inhibiting aldosterone effect (NSAID, spironolactone, and triamterene).


Aldosterone Deficiency: Hyporeninemic hypoaldosteronism - Commonly seen in patients with renal insufficiency (diabetic kidney disease, chronic tubulointerstitial disease, or glomerulonephritis) and those that take certain medications (non-steroidal anti-inflammatory drugs, calcineurin inhibitors).[1] Angiotensin inhibitors - angiotensin-converting enzyme (ACE) inhibitors, angiotensin II receptor blockers (ARBs), direct renin inhibitors Heparin therapy (including low molecular weight heparin) - Heparin has a direct toxic effect on the adrenal zona glomerulosa cells which leads to a reduction in plasma aldosterone concentration.[9] Primary adrenal insufficiency (Addison’s disease) - Associated with the lack of cortisol and aldosterone. This can result from autoimmune adrenalitis, infectious adrenalitis, and other disorders.[14] Critical illness - There is decreased adrenal production of aldosterone and stress-induced hypersecretion of ACTH which can diminish aldosterone synthesis by diverting substrate to the production of cortisol. Congenital isolated hypoaldosteronism - Deficiency of enzymes required for aldosterone synthesis.[14] Pseudohypoaldosteronism type 2 (Gordon’s syndrome or familial hyperkalemic hypertension) - Abnormalities in WNK kinases in the distal nephron increase chloride reabsorption leading to reduced renal potassium secretion. Characterized by hypertension, hyperkalemia, metabolic acidosis, normal renal function, and low or low-normal plasma renin activity and aldosterone concentrations.[14][2] Aldosterone Resistance: Inhibitors of the epithelial sodium channel - Most commonly associated with the administation of potassium-sparing diuretics (spironolactone, eplerenone, amiloride) and certain antibiotics (trimethoprim, pentamidine). Pseudohypoaldosteronism type 1 - Characterized by marked elevations of plasma aldosterone levels. There is an autosomal recessive form, and an autosomal dominant or sporadic form. The autosomal dominant form tends to be associated with milder symptoms