Hyperaldosteronism

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Hyperaldosteronism
Classification and external resources
Aldosterone-2D-skeletal.svg
ICD-10E26
ICD-9255.1
OMIM103900 605635
DiseasesDB6187
MedlinePlus000330
MeSHD006929
 
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Hyperaldosteronism
Classification and external resources
Aldosterone-2D-skeletal.svg
ICD-10E26
ICD-9255.1
OMIM103900 605635
DiseasesDB6187
MedlinePlus000330
MeSHD006929

Hyperaldosteronism, also aldosteronism,[1] is a medical condition wherein too much aldosterone is produced by the adrenal glands, which can lead to lowered levels of potassium in the blood also known as hypokalemia.

Types[edit]

In endocrinology, the terms primary and secondary are used to describe the abnormality (e.g., elevated aldosterone) in relation to the defect, i.e., the tumor's location.

Primary[edit]

Main article: Primary aldosteronism

Primary aldosteronism (hyporeninemic hyperaldosteronism) was previously thought to be most commonly caused by an adrenal adenoma, termed Conn's syndrome. However, recent studies have shown that bilateral idiopathic adrenal hyperplasia is the cause in up to 70% of cases.[citation needed] Differentiating between the two is important, as this determines treatment. Also see congenital adrenal hyperplasia. Adrenal carcinoma is an extremely rare cause of primary hyperaldosteronism. Two familial forms have been identified: Type I ( dexamethasone suppressible ) and Type II ( that has been linked to 7p22.[2] )

Features

Investigations

Management

Secondary[edit]

Secondary refers to an abnormality that indirectly results in pathology through a predictable physiologic pathway, i.e., a renin-producing tumor leads to increased aldosterone, as the body's aldosterone production is normally regulated by renin levels.

One cause is a juxtaglomerular cell tumor. Another is renal artery stenosis, in which the reduced blood supply across the juxtaglomerular apparatus stimulates the production of renin. Also, fibromuscular hyperplasia may cause secondary hyperaldosteronism. Other causes can come from the tubules: Hyporeabsorption of sodium (as seen in Bartter and Gitelman syndromes) will lead to hypovolemia/hypotension, which will activate the RAA system.

Symptoms[edit]

It can be asymptomatic, but the following symptoms may be present:

Diagnostic workup[edit]

When taking a blood test, the aldosterone-to-renin ratio is abnormally increased in primary hyperaldosteronism, and decreased or normal but with high renin in secondary hyperaldosteronism.

See also[edit]

Treatment[edit]

Treatment includes Spironolactone, a potassium-sparing diuretic that works by acting as an aldosterone antagonist.

References[edit]

External links[edit]