Aldosterone, 24-Hour Urine

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Turnaround Time: 6 - 9 days
CPT Code:


Test Type: 10 mL Urine (24-hour)
Stability Time:



Room temperature

7 days


14 days


14 days

Freeze/thaw cycles

Stable x3

Reference Range:

• 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


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.

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. Demers RM, Whitley RJ. Function of the adrenal cortex. In Burtis CA, Ashwood ER, eds. Tietz Textbook of Clinical Chemistry. Philadelphia, Pa: WB Saunders Co;1999:1530-1569.

2. Connell JM, Davies E. The new biology of aldosterone. J Endocrinol. 2005 Jul; 186(1):1-20. PubMed 16002531

3. Atlas SA. The renin-angiotensin aldosterone system: Pathophysiological role and pharmacologic inhibition. J Manag Care Pharm. 2007 Oct; 13(8 Suppl B):S9-S20. PubMed 17970613

4. Ten S, New M, Maclaren N. Clinical Review 130: Addison's disease 2001. J Clin Endocrinol Metab. 2001 Jul; 86(7):2909-2922. PubMed 11443143

5. Funder JW, Carey RM, Fardella C, et al. Case detection, diagnosis, and treatment of patients with primary aldosteronism: An Endocrine Society clinical practice guideline. J Clin Endocrinol Metab. 2008 Sep; 93(9):3266-3281. PubMed 18552288

6. Vasan RS, Evans JC, Larson MG, et al. Serum aldosterone and the incidence of hypertension in nonhypertensive persons. N Engl J Med. 2004 Jul 1; 351(1):33-41. PubMed 15229305

7. Stowasser M, Taylor PJ, Pimenta E, et al. Laboratory investigation of primary aldosteronism. Clin Biochem Rev. 2010 May; 31(2):39-56. PubMed 20498828

Bravo EL. Primary aldosteronism. Issues in diagnosis and management. Endocrinol Metab Clin North Am. 1994 Jun; 23(2):271-283. PubMed 8070422

Young WF Jr. Pheochromocytoma and primary aldosteronism: Diagnostic approaches. Endocrinol Metab Clin North Am. 1997 Dec; 26(4):801-827. PubMed 9429861

Collection Details:

Patient Preparation:

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.

Collection Instructions:

Instructions for suppression/stimulation tests that involve serum aldosterone measurement can be found in the online Endocrine Appendix: Aldosterone Suppression.

Plastic urine container with no preservative.

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.