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Related to hyperaldosteronism: Hypoaldosteronism, Secondary hyperaldosteronism




Hyperaldosteronism is a disorder which is defined by the body's overproduction of aldosterone, a hormone that controls sodium and potassium levels in the blood. Its overproduction leads to retention of salt and loss of potassium, which leads to hypertension (high blood pressure).


Also known as Conn's syndrome, primary aldosteronism, and secondary aldosteronism, this disorder takes several forms. It often begins with a tumor that produces aldosterone. In fact, approximately 60-70% of the cases of primary aldosteronism result from tumors in the adrenal gland area. Aldosterone is normally produced by the adrenal cortex, or the outer portion of the gland that rests on top of each kidney. Primary aldosteronism is due to adenoma, a typically benign tumor in which the cells form to act as glands or cause the glands on which they rest to overproduce. It can cause a number of problems, most notably hypertension. In secondary aldosteronism, factors outside the adrenal gland may cause overproduction of aldosterone, or overproduction of renin, an enzyme stored in the kidney area that stimulates aldosterone and raises blood pressure. Obstructive renal artery disease may also cause hypertension from elevated renin stimulating aldosterone. Oral contraceptives have been known to increase the secretion of aldosterone in some patients. This disorder is more common in women.

Causes and symptoms

Hyperaldosteronism is most often caused by the invasion of adenoma. Other adrenal cancers and hyperplasia, or the increase in the bulk of an organ due to increased cell production, may also cause hyperaldosteronism. Those diseases and factors influencing the adrenal and kidney functions may lead to secondary aldosteronism. The primary symptom of hyperaldosteronism is moderate hypertension, or high blood pressure. In addition, a patient may experience orthostatic hypotension, or reduced blood pressure when a person stands after lying down. Constipation, muscle weakness (sometimes to the point of periodic paralysis), excessive urination, excessive thirst, headache, and personality changes are also possible symptoms. Some patients will show no obvious symptoms.


Screening tests can be conducted to pinpoint a diagnosis of hyperaldosteronism. If a patient is taking drugs to reduce high blood pressure, the physician may order these drugs stopped for a time period before conducting tests, since these drugs will affect results. Blood and urine tests may be conducted to check for levels of aldosterone, potassium levels, or renin activity. A computed tomography scan (CT scan) may be ordered to detect tumors as small as five to seven mm. These combined tests approach 95% accuracy for detecting aldosterone-producing adenoma. Laboratory findings recording blood pressure, edema, and aldosterone and plasma renin activity can help the physician differentiate between primary aldosteronism and secondary aldosteronism.


Once the physician has made a diagnosis of hyperaldosteronism, the adrenal glands should be checked for possible adenomas. This can be done through imaging or with a surgical dissection of the gland. Surgical or ablative treatment will vary depending on the number of tumors found. Since more than 60% of hyperaldosteronism cases are caused by these tumors, treatment of the tumors will help eliminate the resulting high blood pressure in many patients. Some patients will receive antihy-pertensive drugs, like calcium channel blockers, to control high blood pressure. The use of diuretics can help control hypertension by reducing volume. Potassium levels should be considered in the type of diuretic ordered and the levels should be checked throughout treatment. The most widely used drug for treatment of hyperaldosteronism is spironolactone. This drug helps control aldosterone, but should not be prescribed for some patients, especially those with certain kidney diseases. Spironolactone has several possible adverse effects, depending on the dosage. In all cases of hyperaldosteronism, the treatment should be carefully based on the specific type or underlying cause of the disorder.

Alternative treatment

Patients may choose to work with their physician or alternative provider to control hypertension with diet, stress reduction (including massage, meditation, biofeedback, and yoga), and other remedies. Blood pressure elevation needs to be controlled and monitored by frequent blood pressure measurements. There is no alternative treatment known for the underlying adenoma.


Hyperaldosteronism carries with it all the possible complications of high blood pressure, including thickening of arterial walls and a higher risk of angina, kidney failure, stroke, or heart attack. Another possible, and less reversible complication than hypertension, is kidney damage. When primary aldosteronism is caused by a solitary adenoma, the prognosis is good. Once this tumor is removed, blood pressure will drop, and 70% of these patients have full remission. Patients whose hyperaldosteronism results from adrenal hyperplasia will remain hypertensive. However, in up to 70% of patients, blood pressure can be reduced somewhat with drug therapy. Many patients will be faced with the prospect of controlling their hypertension for the remainder of their lives.


There is no known prevention for most causes of hyperaldosteronism.

Key terms

Ablative — Used to describe a procedure involving removal of a tissue or body part, or destruction of its function.
Adenoma — A growth of cells, usually a benign tumor, that forms a gland or gland-like substance. These tumors can secrete hormones or cause changes in hormone production in nearby glands.
Adrenal — Refers to the glands which sit on top of each kidney and that secrete various hormones.
Antihypertensive — Used to describe drugs or treatments designed to control hypertension, or high blood pressure.
Diuretic — A substance or drug that is taken to promote the formation and release of urine. In the treatment of high blood pressure, diuretics can help reduce the overall fluid volume in the body.
Renal — Relating to the kidney. The renal artery is one of two branches of the large blood vessel in the stomach area that serves the kidneys, ureters (tubes that carry urine from the kidney to the bladder) and adrenal glands.



American Heart Association. 7320 Greenville Ave. Dallas, TX 75231. (214) 373-6300. http://www.americanheart.org.
American Society of Hypertension. 515 Madison Ave., Suite 1212, New York, NY 10022. (212) 644-0650. http://www.ash-us.org.
National Heart, Lung and Blood Institute. PO Box 30105, Bethesda, MD 20824-0105. (301) 251-1222. http://www.nhlbi.nih.gov.


Hypertension Network. 〈http://www.bloodpressure.com〉.


 [al-dos´ter-ōn-izm″, al″do-ster´ōn-izm]
an abnormality of electrolyte metabolism produced by excessive secretion of aldosterone, it may be primary or occur secondarily in response to extra-adrenal disease. There may be hypertension, hypokalemia, alkalosis, muscular weakness, polyuria, and polydipsia. Called also hyperaldosteronism.
primary aldosteronism that arising from oversecretion of aldosterone, characterized typically by hypokalemia, alkalosis, muscular weakness, polyuria, polydipsia, hypertension, cardiac irregularity, and tetany. The most common etiologic factors are adrenal adenoma, idiopathic hyperplasia of the adrenal cortex, and occasionally carcinoma of the adrenal gland. Most adenomas affect only one of the two glands and therefore can be removed surgically without depriving the patient of a sufficient supply of adrenal cortical hormones. If removal of both glands is necessary, this creates a serious and potentially fatal insufficiency of the hormones. Called also Conn's syndrome.
pseudoprimary aldosteronism that caused by bilateral adrenal hyperplasia and having the same signs and symptoms as primary aldosteronism.
secondary aldosteronism that due to extra-adrenal stimulation of aldosterone secretion; it is commonly associated with edematous states, as in nephrotic syndrome, hepatic cirrhosis, heart failure, and accelerated hypertension.


A disorder caused by excessive secretion of aldosterone.
Synonym(s): hyperaldosteronism


/hy·per·al·dos·ter·on·ism/ (-al-dos´tĕ-ro-nizm) aldosteronism.


(hī′pər-ăl-dŏs′tə-rō-nĭz′əm, -ăl′dō-stĕr′ə-)



Conn syndrome, primary aldosteronism, Endocrinology A condition caused by overproduction of aldosterone by an adrenal cortex tumor, resulting in ↓ K+, sodium retention, arrhythmias, alkalosis, muscle weakness, polydipsia, polyuria, HTN


A disorder caused by excessive secretion of aldosterone.
Synonym(s): hyperaldosteronism.


The effect of excessive output of ALDOSTERONE from the outer layer (cortex) of the adrenal gland. There is muscle weakness from potassium deficiency, excessive urine output and consequent great thirst, and high blood pressure (HYPERTENSION). When the condition is due to a tumour of the aldosterone-secreting cells it is called Conn's syndrome.


an abnormality of electrolyte metabolism produced by excessive secretion of aldosterone; it may be primary (Conn's syndrome) or occur secondarily in response to extra-adrenal disease. There may be hypertension, hypokalemia, alkalosis, muscular weakness, polyuria and polydipsia. Called also aldosteronism.
References in periodicals archive ?
In humans, six different primary hyperaldosteronism subtypes have been identified, including familial hyperaldosteronism.
Primary mineralocorticoid excess-primary hyperaldosteronism.
The gross features of familial hyperaldosteronism are scarcely reported in the literature.
Previously, researchers believed that hyperaldosteronism was a rare feature in people with hypertension since it apparently affected only 1 to 2 percent of people with hypertension.
Adrenal myelolipoma associated with primary hyperaldosteronism.
Regardless of signs or symptoms, perform screening laboratory tests for 3 types of adrenal hyperfunction: hypercortisolism, hyperaldosteronism, and hypersecretion of catecholamines (pheochromocytoma).
Hence, the likely cause of hypokalaemia is either primary tubular defect or hyperaldosteronism due to excess urinary sodium loss.
The exclusion criteria were: history of secondary hypertension, such as hyperaldosteronism, pheochromocytoma, renal artery stenosis, cushing syndrome; presence of target-organ damage (renal failure, congestive heart failure, myocardial infarction or cerebrovascular accident 6 months preceeding to the study), second- or third-degree heart block, valvular heart disease; diabetic subjects; hepatic dysfunction; any disease state which judged by the investigator could interfere with trial participation or trial evaluation; known or suspected allergy to the trial product or the related products; and participation in any other clinical studies within 30 days prior to screening.
10) Further complications have been reported when excessive gastrointestinal losses of water and sodium trigger increased renin secretion and secondary hyperaldosteronism results.
A novel genetic locus for low renin hypertension: familial hyperaldosteronism type II maps to chromosome 7 (7p22).