Aldosterone, 24-Hour Urine

Urine (24-hour)

10 mL

1 mL (Note: This volume does not allow for repeat testing.)

Plastic urine container with no preservative (Note: 1 g/L boric acid may be added as a preservative for other test without harm to aldosterone.)

If patient is taking diuretics, antihypertensive drugs, cyclic progestational agents, estrogen, or licorice, results for aldosterone may not be interpretable. Patient should be on a diet containing 135 mmol (3 g) sodium per day for at least two weeks and preferably 30 days prior to testing.

Study of adrenocortical-renin-angiotensin system; adrenal cortical function test; evaluate renal hypertension; diagnose Conn syndrome (primary aldosteronism); evaluate hypokalemia with hypertension

Urinary aldosterone measurements alone are of limited value in the diagnosis of hyperaldosteronism. Elevated levels mandate further investigation.

This test was developed and its performance characteristics determined by Labcorp. It has not been cleared or approved by the Food and Drug Administration.

Liquid chromatography/tandem mass spectrometry (LC/MS-MS)

• Pediatric:^1,2

− 0 to 3 days: 0.00−5.00 μg/24 hours

− 4 days to 10 years: 0.00−8.00 μg/24 hours

− >10 years: 0.00−19.00 μg/24 hours

• Adults:

− Low sodium intake: 20.00−80.00 μg/24 hours

− Normal sodium intake: 0.00−19.00 μg/24 hours

− High sodium intake: 0.00−12.00 μg/24 hours

The renin-angiotensin system and potassium ion are the major regulators of aldosterone secretion, whereas ACTH and other POMC peptides, sodium ion, vasopressin, dopamine, ANP, α-adrenergic agents, serotonin, and somatostatin are minor modulators.^1,2 Renin cleaves angiotensinogen, which is synthesized by the liver; to produce angiotensin I. Angiotensin I is, in turn, rapidly cleaved by angiotensin-converting enzyme (ACE) in the lung and other tissues to form angiotensin II. Angiotensin II stimulates aldosterone secretion and vasoconstriction. Factors that decrease renal blood flow, such as hemorrhage, dehydration, salt restriction, upright posture, and renal artery narrowing, increase renin levels which, in turn, raise aldosterone levels. In contrast, factors that increase blood pressure, such as high salt intake, peripheral vasoconstrictors and supine posture, decrease renin and aldosterone levels.³ Aldosterone promotes active sodium transport and excretion of potassium.

Hypokalemia increases and hyperkalemia decreases renin release.¹ Potassium also directly increases aldosterone secretion by the adrenal cortex and aldosterone then lowers serum potassium by stimulating its excretion by the kidney. High dietary potassium intake increases plasma aldosterone and enhances the aldosterone response to a subsequent potassium or angiotensin II infusion.³

Primary hyperaldosteronism, also referred to as Conn syndrome, is caused by the overproduction of aldosterone by one or both of the adrenal glands.^1,2 Historically, primary aldosteronism was considered to be an uncommon cause of hypertension. However, recent studies indicate that 10% to 15% of cases are associated with primary hyperaldosteronism.⁴ Secondary hyperaldosteronism is relatively common and can occur as the result of any condition that decreases blood flow to the kidneys (ie, renal artery stenosis), decreases blood pressure, or lowers plasma sodium levels. Secondary hyperaldosteronism may also be seen with cirrhosis, congestive heart failure, and toxemia of pregnancy.

Hyperaldosteronism increases reabsorption of sodium and loss of potassium by the kidneys, resulting in an electrolyte imbalance.^1,5 The condition can be asymptomatic, although muscle weakness can occur if potassium levels are very low. A number of studies have suggested that high-normal aldosterone levels predict development of high blood pressure in normotensive subjects⁶ and that increased aldosterone action contributes to hypertension, cardiovascular fibrosis, and cardiac hypertrophy.^5-7