Aldosterone, Right Adrenal Vein, Serum
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)
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 is not a major factor in regulating aldosterone secretion.
See Steroid Pathways in Special Instructions.
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.
No established reference values.
A high ratio of serum aldosterone (SA) in ng/dL to plasma renin activity (PRA) in ng/mL per hour, is a positive screening test result, a finding that warrants further testing. An SA/PRA ratio > or =20 is only interpretable with an SA > or =15 ng/dL and indicates probable primary aldosteronism.
Renal disease, such as unilateral renal artery stenosis, results in elevated renin and aldosterone levels. Renal venous catheterization may be helpful. A positive test is a renal venous renin ratio (affected/normal) >1.5.
See Renin-Aldosterone Studies and Steroid Pathways 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 should be discontinued for 4 to 6 weeks before testing.
Late p.m. levels can be up to 30% lower than early a.m. levels. Supine values are on average 50% lower than upright collections. Sodium deplete subjects have significantly elevated serum aldosterone (SA) levels, potentially exceeding the upper limit of the salt replete upright reference range by several fold. To account for these variables, at least in part, it is recommended that PRA is measured concomitantly. In situations of physiological variability, PRA should be altered in the same direction as aldosterone. See Renin-Aldosterone Studies in Special Instructions.
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 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.
Clinical Reference 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 1997;26:801-827
3. Hurwitz S, Cohen RJ, Williams GH: Diurnal variation of aldosterone and plasma renin activity: timing relation to melatonin and cortisol and consistency after prolonged bed rest. J Appl Physiol 2004;96:1406-1414