Wallach's Interpretation of Diagnostic Tests: Pathways to Arriving at a Clinical Diagnosis (1125 page)

   Hypertension due to unilateral renal artery stenosis or unilateral renal parenchymal disease.

   Increased plasma volume due to high-sodium diet, administration of salt-retaining steroids.

   Eighteen to twenty-five percent of essential hypertensives (low-renin essential hypertension) and 6% of normal controls.

   Advancing age in both normal and hypertensive patients (decrease of 35% from the third to the eighth decade).

   May also be decreased in CAH secondary to 11-hydroxylase or 17-hydroxylase deficiency with oversecretion of other mineralocorticoids.

   Rarely in Liddle syndrome and excess licorice ingestion.

   Use of various drugs (propranolol, clonidine, reserpine; slightly with methyldopa).

   Usually cannot be stimulated by salt restriction, diuretics, and upright posture that deplete plasma volume; therefore, measure before and after furosemide and 3–4 hours of ambulation.

   Limitations

   The plasma renin activity cannot be interpreted if the patient is being treated with spironolactone (Aldactone). Spironolactone should be discontinued for 4–6 weeks before testing.

   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-to-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 depends on the isotope administered, the dose given, and the clearance rate in the individual patient.