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Classification and external resources
Specialty endocrinology
ICD-10 E26
ICD-9-CM 255.1
OMIM 103900 605635
DiseasesDB 6187
MedlinePlus 000330
eMedicine radio/354
Patient UK Hyperaldosteronism
MeSH D006929

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 (hypokalemia) and increased hydrogen ion excretion (alkalosis).

The most common cause of mineralocorticoid excess is primary hyperaldosteronism reflecting excess production of aldosterone by adrenal zona glomerulosa. Bilateral micronodular hyperplasia is more common than unilateral adrenal adenoma.

Video explanation

Signs and symptoms[edit]

It can be asymptomatic, but these symptoms may be present:


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. Hyperaldosteronism can also be caused by plant poisoning, where the patient has been exposed to too much licorice. Licorice a perennial herb that is used in making candies and in cooking other desserts because of its sweet taste. It contains the chemical glycyrrhizin that has medicinal uses, but at higher levels it can be toxic. It has the potential for causing problems with sodium and potassium in the body. It also interferes with the enzyme in the kidneys that converts cortisol to cortisone.


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. 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.)[3]




  • Adrenal adenoma: surgery
  • Bilateral adrenocortical hyperplasia: aldosterone antagonist, e.g., spironolactone


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. Likewise, fibromuscular dysplasia may cause stenosis of the renal artery, and therefore 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 RAAS.


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.


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

See also[edit]


External links[edit]