Aldosterone with Sodium, Urine

CPT CODE:

USEFUL FOR:

Investigation of 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's syndrome)

SPECIMEN REQUIRED:

16 mL from a 24-hour urine collection. Add 25 mL of 50% acetic acid as preservative at start of collection. Use 15 mL of 50% acetic acid for children <5 years old. This preservative is intended to achieve a pH of between approximately 2 and 4.  See "Urine Preservatives" in Special Instructions for multiplecollections and "Renin - Aldosterone Studies" in Special Instructions for more detailed instructions. Place 11 mL in a plastic, 13-mL urine tube and label as "Aldosterone." Place 5 mL in a plastic, 13-mL urine tube and label as "Sodium." Send specimen refrigerated.  Note:    24-Hour volume is required on request form for processing.  Urine Preservative Collection OptionsNote:  The addition of preservative or application of temperature controls must occur within 4 hours of completion of the collection.
Ambient:                     YesRefrigerated:              YesFrozen:                        Yes6N HCl:                        No50% Acetic Acid:     PreferredNa(2)CO(3):               NoToluene:                      Yes6N HNO(3):                NoBoric Acid:                 YesThymol:                       Yes

TRANSPORT TEMPERATURE:

Refrig\Frozen OK\Ambient OK with preservative

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 subjects 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 corticalhyperplasia, is characterized by hypertension accompanied byincreased aldosterone levels, hypernatremia, and hypokalemia.Secondary hyperaldosteronism (eg, in response to renovasculardisease, salt depletion, potassium loading, cardiac failure withascites, pregnancy, Bartter's syndrome) is characterized byincreased aldosterone levels and increased plasma rennin activity.

CLINICAL INTERPRETATION:

Under normal circumstances, if the 24-hour urinary sodiumexcretion is >200 mEq, the urinary aldosterone excretion shouldbe <10 ug/24 hours.
Urinary aldosterone excretion >12 ug/24 hours as part of an aldosterone suppression test is consistent with hyperaldosteronism.
24-Hour urinary sodium excretion should exceed 200 mEq to document adequate sodium repletion.
See "Renin - Aldosterone Studies" under Special Instructions. Note:  Advice on stimulation or suppression tests is available                from Mayo Clinic's Division of Endocrinology and may                be obtained by calling Mayo Medical Laboratories.

REFERENCE VALUES:

ALDOSTERONE

      0-30 days:  0.7-11.0 ug/24h*

      1-11 months:  0.7-22.0 ug/24h*

      > or = 1 year:  2.0-20.0 ug/24h

*Loeuille GA, Racadot A, Vasseur P, Vandewalle B:  Blood and

urinary aldosterone levels in normal neonates, infants and children.

Pediatrie 1981;36:335-344

SODIUM

      40-217 mmol/24h

If the 24-hour urinary sodium excretion is >200 mmol, the urinary

aldosterone excretion should be <10 ug.