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Values are valid only on day of printing. |
Investigation using inferior vena cava specimen for:
-Primary aldosteronism (eg, adrenal adenoma/carcinoma and adrenal cortical hyperplasia)
-Secondary aldosteronism (renovascular disease, salt depletion, potassium loading, cardiac failure with ascites, pregnancy, Bartter syndrome)
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.
No established reference values.
A high ratio of plasma aldosterone (PA) 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. A PA:PRA ratio of20 or greater is only interpretable with a PA of 15 ng/dL or greater 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) above1.5.
The following are available 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 800-533-1710.
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-depleted subjects have significantly elevated plasma aldosterone (PA) 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 plasma renin activity (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 finding of a detectable PRA level or a low PA:PRA ratio does not exclude the diagnosis of primary aldosteronism. In addition, in a patient taking an ACE inhibitor, an undetectably low PRA level is a strong predictor for primary aldosteronism.
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