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HelpEpic Test Code LAB354 Aldosterone, 24 Hour, Urine
Additional Codes
MML Code: ALDU
NY State Approved
YesPerforming Laboratory
Mayo Clinic Laboratories in Rochester
Reporting Name
Aldosterone, UMethod Name
Liquid Chromatography Tandem Mass Spectrometry (LC-MS/MS)
Specimen Stability Information
| Specimen Type | Temperature | Time | Special Container |
|---|---|---|---|
| Urine | Refrigerated (preferred) | 28 days | |
| Frozen | 28 days | ||
| Ambient | 14 days |
Ordering Guidance
Advice on stimulation or suppression tests is available from Mayo Clinic's Division of Endocrinology; call 800-533-1710.
Necessary Information
24-Hour volume (in milliliters) is required.
Specimen Required
Patient Preparation: Spironolactone (Aldactone) should be discontinued for 4 to 6 weeks before specimen collection. The plasma renin activity cannot be interpreted if the patient is being treated with spironolactone.
Supplies: Urine tubes, 10 mL (T068)
Container/Tube: Plastic, urine tube
Specimen Volume: 10 mL
Collection Instructions:
1. Add 25 mL of 50% acetic acid as preservative at start of collection. Use 15 mL of 50% acetic acid for children under the age of 5 years. This preservative is intended to achieve a pH of between approximately 2 and 4.
2. Collect urine for a full 24 hours (required) and record the total volume.
Additional Information: See Urine Preservatives-Collection and Transportation for 24-Hour Urine Specimens for multiple collections.
Specimen Type
UrineSpecimen Minimum Volume
1 mL
Reference Values
0-30 days: 0.7-11.0 mcg/24 h*
31 days-11 months: 0.7-22.0 mcg/24 h*
≥1 year: 2.0-20.0 mcg/24 h
*Loeuille GA, Racadot A, Vasseur P, Vandewalle B. Blood and urinary aldosterone levels in normal neonates, infants and children. Pediatrie. 1981;36(5):335-344
For International System of Units (SI) conversion for Reference Values, see www.mayocliniclabs.com/order-tests/si-unit-conversion.html
Report Available
2 to 8 daysDay(s) Performed
Tuesday, Thursday
CPT Code Information
82088
Reject Due To
All specimens will be evaluated at Mayo Clinic Laboratories for test suitability.Useful For
Investigating primary aldosteronism (eg, adrenal adenoma/carcinoma and adrenal cortical hyperplasia) and secondary aldosteronism (renovascular disease, salt depletion, potassium loading, cardiac failure with ascites, pregnancy, Bartter syndrome) using 24-hour urine collections
Special Instructions
Clinical Information
Aldosterone stimulates sodium transport across cell membranes, particularly in the distal renal tubule where sodium is exchanged for hydrogen and potassium. Secondarily, aldosterone is important in the maintenance of blood pressure and blood volume.
Aldosterone is the major mineralocorticoid and is produced by the adrenal cortex. The renin-angiotensin system is the primary regulator of the synthesis and secretion of aldosterone. Likewise, increased concentrations of potassium in the plasma may directly stimulate adrenal production of the hormone. Under physiologic conditions, pituitary adrenocorticotropic hormone can stimulate aldosterone secretion.
Urinary aldosterone levels are inversely correlated with urinary sodium excretion. Normal individuals will show a suppression of urinary aldosterone with adequate sodium repletion.
Primary hyperaldosteronism, which may be caused by aldosterone-secreting adrenal adenoma/carcinomas or adrenal cortical hyperplasia, is characterized by hypertension accompanied by increased aldosterone levels, hypernatremia, and hypokalemia. Secondary hyperaldosteronism (eg, in response to renovascular disease, salt depletion, potassium loading, cardiac failure with ascites, pregnancy, Bartter's syndrome) is characterized by increased aldosterone levels and increased plasma rennin activity.
Interpretation
Urinary aldosterone excretion greater than 12 mcg/24 hours as part of an aldosterone suppression test is consistent with hyperaldosteronism.
For more information see Renin-Aldosterone Studies.
Cautions
Angiotensin converting enzyme (ACE) inhibitors have the potential to "falsely elevate" plasma renin activity (PRA). Therefore, in a patient treated with an ACE-inhibitor, the findings of a detectable PRA level or a low sodium aldosterone (SA)/PRA ratio do not exclude the diagnosis of primary aldosteronism. In addition, a strong predictor for primary aldosteronism is a PRA level undetectably low in a patient taking an ACE-inhibitor.