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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 US Food and Drug Administration (FDA).
Liquid chromatography/tandem mass spectrometry (LC/MS-MS)
− 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
− 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
1 mL (Note: This volume does not allow for repeat testing.)
Instruct the patient to void at 8 AM and discard the specimen. Then collect all urine including the final specimen voided at the end of the 24-hour collection period (ie, 8 AM the next morning) into the plastic urine container. Screw the lid on securely. Transport the specimen promptly to the laboratory. Container must be labeled with patient's full name, date and time collection started, and date and time collection finished. pH must be 4 to 8.
Causes for Rejection
Incomplete 24-hour collection; original container with pH <2
Instructions for suppression/stimulation tests that involve serum aldosterone measurement can be found in the online Endocrine Appendix: Aldosterone Suppression.
|Order Code||Order Code Name||Order Loinc||Result Code||Result Code Name||UofM||Result LOINC|
|004291||Aldosterone, Urine||004293||Aldosterone,U, Timed||ug/24 hr||1765-7|
|004291||Aldosterone, Urine||289117||Aldosterone U,Random||ug/L||1764-0|