|Values are valid only on day of printing.|
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)
The renal juxtaglomerular apparatus generates renin, an enzyme that converts angiotensinogen to angiotensin I. The inactive angiotensin I is enzymatically converted to the active octapeptide angiotensin II, a potent vasopressor responsible for hypertension of renal origin. Angiotensin II also stimulates the zona glomerulosa of the adrenal cortex to release aldosterone.
Renin secretion by the kidney is stimulated by a fall in glomerular blood pressure, by decreased sodium concentration at the macula densa at the distal tubule, or by stimulation of sympathetic outflow to the kidney, such as in renal vascular diseases.
0-2 years: 4.6 ng/mL/hour (mean)* Range: 1.4-7.8 ng/mL/hour
3-5 years: 2.5 ng/mL/hour (mean)* Range: 1.5-3.5 ng/mL/hour
6-8 years: 1.4 ng/mL/hour (mean)* Range: 0.8-2.0 ng/mL/hour
9-11 years: 1.9 ng/mL/hour (mean)* Range: 0.9-2.9 ng/mL/hour
12-17 years: 1.8 ng/mL/hour (mean)* Range: 1.2-2.4 ng/mL/hour
Mean data not standardized as to time of day or diet. Infants were supine, children sitting.
Na-depleted, upright (peripheral vein specimen)
18-39 years: 10.8 ng/mL/hour (mean)
2.9-24.0 ng/mL/hour (range)
> or =40 years: 5.9 ng/mL/hour (mean)
2.9-10.8 ng/mL/hour (range)
Na-replete, upright (peripheral vein specimen)
18-39 years: 1.9 ng/mL/hour (mean)
< or =0.6-4.3 ng/mL/hour (range)
> or =40 years: 1.0 ng/mL/hour (mean)
< or =0.6-3.0 ng/mL/hour (range)
*Stalker HP, Holland NH, Kotchen JM, Kotchen TA: Plasma renin activity in healthy children. J Pediatr 1976;89:256-258
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. A SA/PRA ratio > or =20 and SA > or =15 ng/dL 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 in Special Instructions.
The plasma renin activity 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 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.
Not useful for determination of plasma renin concentration.
This test should not be requested in patients who have recently received radioisotopes, therapeutically or diagnostically, because of potential assay interference. A recommended time period before collection cannot be made because it will depend on the isotope administered, the dose given and the clearance rate in the individual patient. Specimens will be screened for radioactivity prior to analysis. Radioactive specimens received in the laboratory will be held and assayed after the radioactivity has sufficiently decayed. This will result in a test delay.
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