Description, Causes and Risk Factors:
Aldosterone: A mineralocorticoid hormone produced by the zona glomerulosa of the adrenal cortex; its major action is to facilitate potassium exchange for sodium in the distal renal tubule, causing sodium re-absorption and potassium and hydrogen loss; the principal mineralocorticoid. It exists in equilibrium with the aldehyde form.
In Medicine, aldosterone deficiency refers to decreased levels of the hormone aldosterone. The term "isolated hypoaldosteronism" is used to describe lowered aldosterone without corresponding changes in cortisol.
Aldosterone's main actions are to regulate intravascular volume and serum electrolytes by controlling sodium absorption and potassium excretion in the distal nephron. Inherited defects in aldosterone biosynthesis thus cause hypovolemia, hyponatremia and hyperkalemia. Defective aldosterone biosynthesis may be caused by congenital adrenal hyperplasia due to 21-hydroxylase deficiency, in which case cortisol biosynthesis is also affected, or as an isolated defect termed aldosterone synthase (corticosterone methyloxidase deficiency). Many mutations have been documented in each of these genes; in general enzymatic activity must be reduced to <1% of normal for aldosterone biosynthesis to be impaired.
Multiple factors regulate aldosterone secretion. Major regulators are the renin-angiotensin system and potassium ion, whereas minor modulators include ACTH (adrenocorticotropic hormone) and other POMC (propiomelanocortin) peptides, sodium ion, dopamine, vasopressin ANP, ?-adrenergic agents, and somatostatin serotonin.
There are several causes for this condition, including primary adrenal insufficiency, congenital adrenal hyperplasia, and medications (certain diuretics, NSAIDs, and ACE inhibitors).
Possible risk factors:
Deficiency in adrenal renin or other components of the autocrine adrenal renin-angiotensin system.
Adrenal gland unresponsiveness to angiotensin II.
Acquired angiotensin-converting enzyme deficiency.
Acquired biosynthetic defects in aldosterone synthesis.
Aldosterone synthase deficiency.
Decreased renal renin production.
Excessive urination and dehydration can occur when adrenal glands do not produce enough of the hormone, aldosterone. Aldosterone deficiency can cause a low sodium level and high potassium level in the blood, which makes the kidneys unable to concentrate urine. This results in excessive urination that can lead to dehydration.
Patients suspected to have aldosterone deficiencyshould be questioned about the use of any drug or the presence of a disease that can impair aldosterone release, such as a nonsteroidal anti-inflammatory drugs (NSAIDs), angiotensin converting enzyme (ACE) inhibitor, cyclosporine, heparin, or the acquired immunodeficiency syndrome (AIDS).
These disorders can be differentiated by measurement of plasma renin activity (PRA) and serum aldosterone and cortisol. These tests should be performed after the administration of a loop diuretic or three hours in the upright position, which will increase renin and aldosterone release in normal, but not in these disease states.
Aldosterone deficiency should be treated with a mineralocorticoid (such as fludrocortisone), as well as possibly a glucocorticoid for cortisol deficiency, if present. Hyporeninemic hypoaldosteronism is amenable to fludrocortisone treatment, but the accompanying hypertension and edema can prove a problem in these patients, so often a diuretic (such as the thiazide diuretic, bendroflumethiazide, or a loop diuretic, such as furosemide) is used to control the hyperkalemia.
NOTE: The above information is educational purpose. The information provided herein should not be used during any medical emergency or for the diagnosis or treatment of any medical condition.
DISCLAIMER: This information should not substitute for seeking responsible, professional medical care.
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