Aldosterone with Sodium, 24 Hour, Urine
Clinical Information Discusses physiology, pathophysiology, and general clinical aspects, as they relate to a laboratory test
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 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.
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 syndrome)
Under normal circumstances, if the 24-hour urinary sodium excretion is >200 mEq, the urinary aldosterone excretion should be <10 mcg/24 hours.
Urinary aldosterone excretion >12 mcg/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 in 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.
Cautions Discusses conditions that may cause diagnostic confusion, including improper specimen collection and handling, inappropriate test selection, and interfering substances
The plasma renin activity (PRA) cannot be interpreted if the patient is being treated with spironolactone (Aldactone). Spironolactone (Aldactone) should be discontinued for 4 to 6 weeks before testing.
Angiotensin converting enzyme (ACE) inhibitors have the potential to "falsely elevate" 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.
Reference Values Describes reference intervals and additional information for interpretation of test results. May include intervals based on age and sex when appropriate. Intervals are Mayo-derived, unless otherwise designated. If an interpretive report is provided, the reference value field will state this.
0-30 days: 0.7-11.0 mcg/24 hours*
1-11 months: 0.7-22.0 mcg/24 hours*
> or =1 year: 2.0-20.0 mcg/24 hours
*Loeuille GA, Racadot A, Vasseur P, Vandewalle B: Blood and urinary aldosterone levels in normal neonates, infants and children. Pediatrie 1981;36:335-344
41-227 mmol/24 hours
If the 24-hour urinary sodium excretion is >200 mmol, the urinary aldosterone excretion should be <10 mcg.
Clinical References Provides recommendations for further in-depth reading of a clinical nature
1. Young WF Jr: Primary aldosteronism: A common and curable form of hypertension. Cardiol Rev 1999;7:207-214
2. Young WF Jr: Pheochromocytoma and primary aldosteronism: diagnostic approaches. Endocrinol Metab Clin North Am 1977;26:801-827