Hyper-aldosteronism
Hyper-aldosteronism: Excerpt from Handbook of Diseases
In hyperaldosteronism (also called aldosteronism), hypersecretion of the mineralocorticoid aldosterone by the adrenal cortex causes excessive reabsorption of sodium and water and excessive renal excretion of potassium.
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-aldosterone 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-aldosterone 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 hormonal contraceptives, and pregnancy.
Secondary hyperaldosteronism may also result from disorders unrelated to hypertension. Such disorders may 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.
Clinical tip Consider primary hyperaldosteronism in those hypertensive patients with spontaneous hypokalemia or significant hypokalemia on modest diuretic dosing.
Diagnosis
Persistently low serum potassium levels in a nonedematous patient who isn’t taking diuretics, doesn’t have obvious GI losses (from vomiting or diarrhea), and has a normal sodium intake suggest hyperaldosteronism.
If hypokalemia develops in a hypertensive patient shortly after starting treatment with potassium-wasting diuretics (such as thiazides), and if it persists after the diuretic has been discontinued and potassium replacement therapy has been instituted, evaluation for hyperaldosteronism is necessary.
A low plasma renin level that fails to increase appropriately during volume depletion (upright posture, sodium depletion) and a high plasma aldosterone level during volume expansion by salt loading confirm primary hyperaldosteronism in a hypertensive patient without edema.
The serum bicarbonate level is commonly elevated, with ensuing alkalosis due to hydrogen and potassium ion loss in the distal renal tubules.
Other tests show markedly increased urine aldosterone levels and increased plasma aldosterone levels. In secondary hyperaldosteronism, plasma renin levels are increased.
A suppression test is useful to differentiate between primary and secondary hyperaldosteronism. During this test, the patient receives desoxycorticosterone I.M. for 3 days while plasma aldosterone levels and urine metabolites are continuously measured. These levels decrease in secondary hyperaldosteronism but remain the same in primary hyperaldosteronism. Simultaneously, renin levels are low in primary hyperaldosteronism and high in secondary hyperaldosteronism.
Other findings include electrocardiogram signs of hypokalemia (ST-segment depression and flattened U waves), chest X-ray showing left ventricular hypertrophy from chronic hypertension, and localization of the tumor by adrenal angiography, computed tomography scans, or magnetic resonance imaging.
Treatment
The treatment for aldosterone-producing adenoma is unilateral adrenalectomy. Potassium-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.
Special considerations
❑ Monitor and record urine output, blood pressure, weight, and serum potassium levels.
❑ Watch for hypokalemia-induced cardiac arrhythmias, paresthesia, and weakness. Give potassium replacement as ordered.
❑ Ask the dietitian to provide a low-sodium, high-potassium diet.
❑ After adrenalectomy, watch for weakness, hyponatremia, rising serum potassium levels, and signs of adrenal hypofunction, especially hypotension.
❑ If the patient is taking spironolactone or amiloride, advise him to watch for signs of hyperkalemia. Tell him that impotence and gynecomastia may follow long-term use of spironolactone.
❑ Tell the patient who must take steroid hormone replacement to wear a medical identification bracelet.
Book Source Details
- Book Title: Handbook of Diseases
- Author(s): Springhouse
- Year of Publication: 2003
- Copyright Details: Handbook of Diseases, Copyright © 2003 Lippincott Williams & Wilkins.
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Copyright notice for book excerpts: Copyright © 2008 Lippincott Williams & Wilkins. All rights reserved.
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More About This Book:
Title: Handbook of Diseases
Authors: Springhouse
Publisher: Lippincott Williams & Wilkins
Copyright: 2003
ISBN: 1-58255-266-5
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