Hyperaldosteronism - Primary And Secondary

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).

Causes

Hyperaldosteronism may be primary or secondary. Most cases of primary hyperaldosteronism are due to benign aldosterone-producing adrenal adenomas. The remainder are due to bilateral adrenal hyperplasia. Rarely, adrenal carcinoma can cause primary hyperaldosteronism. The incidence is three times higher in women than in men and is highest between ages 30 and 50

In primary hyperaldosteronism, chronic aldosterone excess is independent of the renin-angiotensin system and in fact suppresses plasma renin activity. This aldosterone excess enhances sodium reabsorption by the kidneys, which leads to mild hypernatremia and, simultaneously, hypokalemia and increased extracellular fluid volume. Expansion of intravascular fluid volume also occurs and results in volume-dependent hypertension and increased cardiac output.

Excessive ingestion of English black licorice or licorice-like substances can produce a syndrome similar to primary hyperaldosteronism due to the mineralocorticoid action of glycyrrhizic acid.

Secondary hyperaldosteronism results from an extra-adrenal abnormality that stimulates the adrenal gland to increase production of aldosterone. For example, conditions that reduce renal blood flow (renal artery stenosis) and extracellular fluid volume or produce a sodium deficit activate the renin-angiotensin system and, subsequently, increase aldosterone secretion. Thus, secondary hyperaldosteronism may result from conditions that induce hypertension through increased renin production (such as Wilms' tumor), ingestion of oral contraceptives, and pregnancy.

Secondary hyperaldosteronism may also result from disorders unrelated to hypertension. Such disorders mayor may not cause edema. For example, nephrotic syndrome, hepatic cirrhosis with ascites, and heart failure commonly induce edema; Bartter's syndrome and salt-losing nephritis don't.

Signs and symptoms

Most clinical effects of hyperaldosteronism result from hypokalemia, which increases neuromuscular irritability and produces muscle weakness, fatigue, headaches, paresthesia, and intermittent, flaccid paralysis.

Hypokalemia interferes with normal insulin secretion and can worsen glucose control in diabetic patients with hyperaldosteronism. Hypertension and its accompanying complications are also common. Another characteristic finding is loss of renal concentrating ability, resulting in polyuria and polydipsia. Azotemia indicates chronic potassium depletion nephropathy.

Diagnosis

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.

Treatment

The treatment for aldosterone-producing adenoma is unilateral adrenalectomy. Potassiwn-sparing diuretics (spironolactone and amiloride) are used to control hyperaldosteronism in patients with bilateral hyperplasia or those with unilateral adenoma who are unable to undergo surgery.

Treatment of secondary hyperaldosteronism must include correction of the underlying cause.

Prevention

There is no known prevention for most causes of hyperaldosteronism.