hyperaldosteronism

hyperaldosteronism
/huy'peuhr al'doh ster"euh niz'euhm, -al dos"teuhr euh-/, n. Pathol.
aldosteronism.
[1950-55; HYPER- + ALDOSTERONE + -ISM]

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      increased secretion of the hormone aldosterone by the cells of the zona glomerulosa (the outer zone) of the adrenal cortex. The primary actions of aldosterone are to increase retention of salt and water and to increase excretion of potassium by the kidneys and to a lesser extent by the skin and intestine. Hyperaldosteronism may be classified as primary or secondary. Primary hyperaldosteronism (primary aldosteronism) is the unregulated secretion of aldosterone due to an adrenal tumour or hyperplasia of both adrenal glands. The tumours are nearly always benign (adenoma). Secondary hyperaldosteronism (secondary aldosteronism) is caused by disorders that result in loss of sodium (salt) and water from the body and decreased blood flow to the kidneys.

      Primary hyperaldosteronism is characterized by hypertension and low serum potassium concentrations (potassium deficiency), which can cause fatigue, muscle weakness, aches or cramps, and increased thirst and urination. It is a rare cause of hypertension, accounting for fewer than 5 percent of cases. It is diagnosed by finding high concentrations of aldosterone in the serum and urine in the presence of low plasma renin activity (renin is produced in the kidneys; its production is decreased when aldosterone secretion is increased). Primary hyperaldosteronism caused by an adrenal tumour may be distinguished from that caused by adrenal hyperplasia by hormonal and radiologic studies. The former is treated by surgery and the latter by antihypertensive drugs.

      Secondary hyperaldosteronism occurs as a consequence of activation of the normal physiologic mechanisms that maintain salt and water balance, blood volume, and blood flow to the kidneys. When salt and water are lost (i.e., as a result of diarrhea, persistent vomiting, excessive perspiration, or kidney disease (renal system disease)), production of renin, and therefore of angiotensin and aldosterone, increases. Aldosterone then stimulates salt and water reabsorption by the kidneys. The same sequence of events can be initiated by a fall in effective blood volume, as a result of congestive heart failure or cirrhosis of the liver, or by a fall in blood flow to a kidney, as a result of narrowing of a renal artery. In all these situations, successful treatment of the primary disease leads to a restoration of normal renin, angiotensin, and aldosterone production. If treatment is unsuccessful, then drugs that block the action of aldosterone on the kidneys, such as spironolactone or eplerenone, can be given. Most patients with secondary hyperaldosteronism do not have hypertension or low serum potassium concentrations; the exception is patients with renal artery disease.

Robert D. Utiger
 

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Universalium. 2010.

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