PRA, Plasma Renin Activity

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Fasting Required

Details

Measures the enzymatic activity of renin by assessing how much angiotensin I is generated in plasma over time. Reflects renin-angiotensin system activity.

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PRA Plasma Renin Activity Test Information Guide

Why is it done?
- Measures the enzyme renin produced by the kidneys in response to decreased blood pressure or sodium levels
- Evaluates the renin-angiotensin-aldosterone system (RAAS) function for blood pressure regulation
- Diagnoses secondary hypertension, particularly renovascular hypertension and renal artery stenosis
- Investigates primary aldosteronism (Conn's syndrome) and helps establish the aldosterone-to-renin ratio
- Assesses causes of hypokalemia (low potassium) and electrolyte imbalances
- Performed when evaluating resistant hypertension or hypertension in young patients
- Used to differentiate between different causes of secondary hypertension
Normal Range
- Upright Position (normal): 1.0 to 3.0 ng/mL/hour (or ng/mL/hr)
- Supine Position (normal): 0.1 to 0.3 ng/mL/hour
- Note: Normal ranges vary by laboratory and measurement methods (direct vs. indirect). Reference values may range from approximately 0.4 to 3.0 ng/mL/hour depending on methodology and patient position.
- Interpretation:
- Normal Result: RAAS is functioning appropriately; renin levels respond normally to changes in posture and sodium status
- High Result: Elevated renin production; may indicate renovascular hypertension, renal artery stenosis, renin-secreting tumor, or secondary aldosteronism
- Low Result: Suppressed renin activity; may indicate primary aldosteronism, Cushing's syndrome, or excessive sodium intake
- Units: ng/mL/hour (nanograms per milliliter per hour) or mIU/L (milli-International Units per liter), depending on laboratory
Interpretation
- Elevated Plasma Renin Activity (>3.0 ng/mL/hour):
- • Renovascular hypertension (renal artery stenosis from atherosclerosis or fibromuscular dysplasia)
- • Renin-secreting tumors (juxtaglomerular cell carcinoma)
- • Secondary aldosteronism
- • Diuretic use or volume depletion
- • Severe hypokalemia with metabolic alkalosis
- • ACE inhibitor or ARB therapy effects
- Suppressed/Low Plasma Renin Activity (<0.5 ng/mL/hour):
- • Primary aldosteronism (autonomous aldosterone secretion suppresses renin)
- • Cushing's syndrome or excessive glucocorticoid therapy
- • Licorice ingestion or apparent mineralocorticoid excess (AME)
- • Excessive sodium intake or volume overload
- • Beta-blocker therapy
- • NSAIDs or other medications affecting renin secretion
- Clinical Context and Aldosterone-to-Renin Ratio (ARR):
- • Low PRA with elevated aldosterone and elevated ARR (typically >20-30) suggests primary aldosteronism
- • Results must be interpreted with concurrent aldosterone levels for diagnostic accuracy
- Factors Affecting Results:
- • Patient posture (upright vs. supine) - renin increases with upright position
- • Sodium intake level
- • Time of day (circadian rhythm)
- • Medications (ACE inhibitors, ARBs, beta-blockers, diuretics, NSAIDs)
- • Pregnancy status
- • Renal and adrenal disease
Associated Organs
- Primary Organs Involved:
- • Kidneys (primary source of renin production from juxtaglomerular cells in afferent arteriole)
- • Adrenal glands (produce aldosterone in response to renin-angiotensin axis)
- • Cardiovascular system (regulates blood pressure and volume)
- Associated Conditions - High PRA:
- • Renovascular hypertension (renal artery stenosis)
- • Chronic kidney disease and renal insufficiency
- • Hypokalemia and metabolic alkalosis
- • Secondary hyperaldosteronism
- • Heart failure, hepatic cirrhosis, and nephrotic syndrome
- • Renin-producing tumors
- Associated Conditions - Low PRA:
- • Primary aldosteronism (Conn's syndrome) - most common cause
- • Cushing's syndrome and glucocorticoid excess
- • Adrenal tumors and adrenal insufficiency
- • Apparent mineralocorticoid excess (AME)
- • Pseudohypoaldosteronism
- Potential Complications Associated with Abnormal Results:
- • Uncontrolled hypertension leading to stroke, MI, and organ damage
- • Hypokalemia and cardiac arrhythmias from electrolyte imbalance
- • Progressive renal disease and chronic kidney disease
- • Left ventricular hypertrophy from sustained hypertension
- • Metabolic alkalosis and acid-base disturbances
Follow-up Tests
- Recommended Follow-up Tests Based on Abnormal PRA:
- • Serum aldosterone level (required to calculate aldosterone-to-renin ratio)
- • 24-hour urine aldosterone and sodium to assess aldosterone excretion
- • Serum electrolytes (sodium, potassium, chloride, CO2) to assess acid-base status
- • Blood pressure monitoring (ambulatory or home BP monitoring)
- • Renal function tests (creatinine, eGFR, BUN)
- Imaging Studies (if renovascular hypertension suspected):
- • Doppler ultrasound of renal arteries
- • CT or MR angiography of renal arteries
- • Captopril renal scan (renal scintigraphy with ACE inhibitor)
- • Renal artery catheter angiography (gold standard, reserved for when intervention planned)
- Adrenal Imaging (if primary aldosteronism suspected):
- • Abdominal CT scan to assess for adrenal adenoma
- • Adrenal venous sampling (AVS) for localization of aldosterone production
- Additional Screening Tests (if endocrine disorders suspected):
- • Plasma cortisol and 24-hour urine free cortisol (Cushing's syndrome evaluation)
- • ACTH level to differentiate pituitary from primary adrenal causes
- • Dexamethasone suppression test (if Cushing's suspected)
- Confirmatory Tests for Primary Aldosteronism:
- • Saline suppression test (IV or oral salt loading)
- • Fludrocortisone suppression test
- • Captopril challenge test (ACE inhibitor stimulation)
- Monitoring Frequency:
- • If diagnosed with secondary hypertension: repeat testing 4-6 weeks after initiating treatment, then every 3-6 months as clinically indicated
- • If primary aldosteronism confirmed: baseline studies, then post-treatment monitoring after surgery or medical therapy
Fasting Required?
- Fasting Status: No strict fasting required
- Important Patient Preparation Requirements:
- • Sodium intake: Follow controlled sodium diet 1-2 weeks before test (2-3g daily) for standardization; specific instructions may be provided by physician
- • Medications to discontinue (typically 2-4 weeks before test unless otherwise instructed):
- ◦ ACE inhibitors and ARBs (can suppress renin)
- ◦ Beta-blockers (reduce renin secretion)
- ◦ Diuretics (elevate renin levels)
- ◦ NSAIDs (affect renin secretion)
- ◦ Licorice (can lower renin)
- ◦ Decongestants and stimulants containing pseudoephedrine or phenylephrine
- Posture Requirements:
- • Upright position test: Patient should be upright (standing or sitting) for at least 1 hour before blood draw
- • Supine position test: Patient recumbent (lying flat) for at least 30 minutes before blood draw
- • Both positions often tested to assess posture-response differential
- Timing Considerations:
- • Morning collection preferred (8-10 AM) due to circadian rhythm of renin secretion
- • Allow 15-20 minutes of rest before blood draw after position change
- General Preparation:
- • Avoid strenuous exercise 24 hours before test
- • Avoid alcohol for 24 hours before test
- • Avoid smoking for at least 4 hours before test (nicotine affects renin)
- • Avoid stimulating beverages (caffeine, energy drinks) on morning of test
- • Remain calm and seated for 5-10 minutes after arrival at laboratory before blood draw
- • Wear comfortable, loose-fitting clothing
- Special Collection Instructions:
- • Sample should be collected into EDTA (lavender) tube and processed promptly
- • Sample should be kept on ice and centrifuged within 30 minutes of collection
- • Plasma should be separated and frozen immediately at -20°C or lower for storage
- • Improper handling may result in falsely elevated or decreased values

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