Recipient(s) will receive an email with a link to 'Plasma Renin Activity (PRA)' and will have access to the topic for 7 days.
Subject: Plasma Renin Activity (PRA)
(Optional message may have a maximum of 1000 characters.)
Renin activity is measured indirectly by the ability of the patient's plasma to generate angiotensin.
Cord blood: 4.0–32.0 ng/mL/hour
Newborn (1–7 days): 2.0–35.0 ng/mL/hour
Child, normal-sodium diet, supine:
1–12 months: 2.4–37.0 ng/mL/hour
1–3 years: 1.7–11.2 ng/mL/hour
3–5 years: 1.0–6.5 ng/mL/hour
5–10 years: 0.5–5.9 ng/mL/hour
10–15 years: 05–3.3 ng/mL/hour
Adult, normal-sodium diet
Supine: 0.2–1.6 ng/mL/hour
Standing: 0.7–3.3 ng/mL/hour
Normal values depend on the laboratory and the patients prevailing Na and K, status of hydration, and posture. Only stimulated values are of practical value in evaluating hypertensive patients.
Particularly useful to diagnose curable hypertension (e.g., primary aldosteronism, unilateral renal artery stenosis).
May help differentiate patients with volume excess (e.g., primary aldosteronism) with low PRA from those with medium to high PRA; if latter group shows marked increase in PRA during captopril test, patients should be worked up for renovascular hypertension, but those with little or no increase are not likely to have curable renovascular hypertension.
Captopril test criteria for renovascular hypertension: stimulated PRA ≥12 μg/L/hour, absolute increase PRA ≥10 μg/L/hour, increase PRA ≥150% (or ≥400% if baseline PRA <3 μg/L/hour).
In children with salt-losing form of congenital adrenal hyperplasia due to 21-hydroxylase deficiency, severity of disease is related to degree of increase. PRA level may serve as guide to adequate mineralocorticoid replacement therapy.
Secondary aldosteronism (usually very high levels), especially malignant or severe hypertension 50–80% of patients with renovascular hypertension (Table 16.66).
Normal or high PRA is of limited value to diagnose or rule out renal vascular hypertension.
Very high PRA is highly predictive but has poor sensitivity.
Low PRA using renin–sodium nomogram in untreated patients with normal serum creatinine is strongly against this diagnosis.
Fifteen percent of patients with essential hypertension (high-renin hypertension)
Renin-producing tumors of the kidney
Reduced plasma volume due to low-sodium diet, diuretics, hemorrhage, Addison disease
Some edematous normotensive states (e.g., cirrhosis, nephrosis, congestive heart failure)
Sodium or potassium loss due to GI disease or in 10% of patients with chronic renal failure
Last half of menstrual cycle (twofold increase)
Erect posture for 4 hours (twofold increase)
Ambulatory patients compared to bed patients
Various drugs (diuretics, ACE inhibitors, vasodilators; sometimes by calcium antagonists and alpha-blockers, e.g., diazoxide, estrogens, furosemide, guanethidine, hydralazine, minoxidil, spironolactone, thiazides)
↑, increased; ↓, decreased; N, normal.
Ninety-eight percent of cases of primary aldosteronism. Usually absent or low and can be increased less or not at all by sodium depletion and ambulation in contrast to secondary aldosteronism. PRA may not always be suppressed in primary aldosteronism; repeated testing may be necessary to establish the diagnosis. Normal PRA does not preclude this diagnosis; it is not a reliable screening test.
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.
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.