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Epic Code LAB354 Aldosterone, 24 Hour, Urine

Important Note

Urine Preservative Guide (link)

Additional Codes

Mayo Code: ALDU

Epic Code: LAB354

Interface Order Alias: 10638

Former Cerner Code: 8709

Performing Laboratory

Mayo Clinic Laboratories in Rochester

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

Specimen Type

Urine
Laboratory Test Directory Note:

Addition of 50% acetic acid prior to start of collection is preferred but not required. 
Refrigeration during and after urine collection is an acceptable means of urine preservation.


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 Minimum Volume

1 mL

Specimen Stability Information

Specimen Type Temperature Time Special Container
Urine Refrigerated (preferred) 28 days
  Frozen  28 days
  Ambient  14 days

Urine Preservative Collection Options

Note: The addition of preservative must occur prior to beginning the collection.

Ambient (no additive)

No

Refrigerate (no additive)

No

Frozen (no additive)

No

50% Acetic Acid

Preferred

Boric Acid

OK

Diazolidinyl Urea

No

6M Hydrochloric Acid

No

6M Nitric Acid

No

Sodium Carbonate

No

Thymol

No

Toluene

No

Reject Due To

  All specimens will be evaluated at Mayo Clinic Laboratories for test suitability.

Day(s) Performed

Tuesday, Thursday

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

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.

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.

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.

Reporting Name

Aldosterone, U

Method Name

Liquid Chromatography Tandem Mass Spectrometry (LC-MS/MS)

Method Description

Samples are spiked with deuterated internal standard and are hydrolyzed overnight with acid. Samples are then neutralized and extracted by solid phase extraction. The extracts are dried, reconstituted, and analyzed by liquid chromatography tandem mass spectrometry.(Taylor RL, Singh RJ. Validation of liquid chromatography-tandem mass spectrometry method for analysis of urinary conjugated metanephrine and normetanephrine for screening of pheochromocytoma. Clin Chem. 2002;48[3]:533-539; Wurth R, Tirosh A, Kamilaris CDC, et al. Volumetric modeling of adrenal gland size in primary bilateral macronodular adrenocortical hyperplasia. J Endocr Soc. 2020;5(1):bvaa162)

CPT Code Information

82088

LOINC Code Information

Test ID Test Order Name Order LOINC Value
ALDU Aldosterone, U 1765-7

 

Result ID Test Result Name Result LOINC Value
8556 Aldosterone, U 1765-7
TM47 Collection Duration (h) 13362-9
VL45 Volume (mL) 3167-4

Report Available

2 to 8 days

Test Classification

This test was developed and its performance characteristics determined by Mayo Clinic in a manner consistent with CLIA requirements. It has not been cleared or approved by the US Food and Drug Administration.

Clinical Reference

1. Young WF Jr. Primary aldosteronism: a common and curable form of hypertension. Cardiol Rev. 1999;7(4):207-214

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

3. Fredline VF, Taylor PJ, Dodds HM, Johnson AG. A reference method for the analysis of aldosterone in blood by high-performance liquid chromatography-atmospheric pressure chemical ionization-tandem mass spectrometry. Analytical Biochem. 1997;252(2):308-313

4. Carey RM, Padia SH. Primary mineralocorticoid excess disorders and hypertension. In: Jameson JL, De Groot LJ, de Kretser DM, Giudice LC, et al, eds. Endocrinology: Adult and Pediatric. 7th ed. WB Saunders; 2016:1871-1891