Plasma renin activity (PRA), angiotensinogenase.
To assist in evaluating for a possible cause of hypertension.
There are no fluid restrictions unless by medical direction. The patient should be on a normal sodium diet (1–2 g sodium per day) for 2 to 4 wk before the test. Inform the patient or family member that the position required (supine or upright) must be maintained for 2 hr before specimen collection. By medical direction, the patient should avoid diuretics, antihypertensive drugs, herbals, cyclic progestogens, and estrogens for 2 to 4 wk before the test. Protocols may vary among facilities.
Method: Enzyme linked immunoassay.
|Age and Position||Conventional Units||SI Units (Conventional Units × 1)|
|Newborn–12 mo||2–35 ng/mL/hr||2–35 mcg/L/hr|
|Supine, normal sodium diet|
|1–3 yr||1.7–11.2 ng/mL/hr||1.7–11.2 mcg/L/hr|
|4–5 yr||1–6.5 ng/mL/hr||1.0–6.5 mcg/L/hr|
|6–10 yr||0.5–5.9 ng/mL/hr||0.5–5.9 mcg/L/hr|
|11–15 yr||0.5–3.3 ng/mL/hr||0.5–3.3 mcg/L/hr|
|Adult||0.2–2.3 ng/mL/hr||0.2–2.3 mcg/L/hr|
|Upright, normal sodium diet|
|Adult–older adult||0.5–4 ng/mL/hr||0.5–4 mcg/L/hr|
|Values vary according to the laboratory performing the test, as well as the patient's age, gender, dietary pattern, state of hydration, posture, and physical activity.|
Critical Findings and Potential Interventions
Overview(Study type: Blood collected in a lavender-top [EDTA] or pink-top [K2-EDTA] tube; related body system: Endocrine and Urinary systems. Specify patient position [upright or supine] and exact source of specimen [peripheral vs. arterial]. Venipuncture should be performed after the patient has been in the upright [sitting or standing] position for 2 hr. If a supine specimen is requested on an inpatient, the specimen should be collected early in the morning before the patient rises. The specimen should be immediately transported in an ice slurry to the laboratory.) Renin is an enzymatic peptide hormone secreted by the granular cells of the juxtaglomerular apparatus in the kidney in response to sodium depletion and hypovolemia. Renin activates the renin-angiotensin system through the conversion of angiotensinogen to angiotensin I. Angiotensin I is converted to the biologically active angiotensin II by angiotensin-converting enzyme primarily within the capillaries of the lungs. Angiotensin II is a powerful vasoconstrictor that ultimately maintains the appropriate perfusion pressure in the kidneys. Angiotensin II stimulates aldosterone production in the adrenal cortex, secretion of antidiuretic hormone from the pituitary, and stimulates the thirst reflex from the hypothalmus. The net effect is regulation of blood pressure by regulating arterial vasoconstriction and the movement of extracellular fluids such as plasma, lymphatic fluid, and interstitial fluid. Excessive amounts of angiotensin II cause renal hypertension. The random collection of specimens without prior dietary preparations does not provide clinically significant information. Values should also be evaluated along with simultaneously collected aldosterone levels (see studies titled "Aldosterone" and "Angiotensin-Converting Enzyme").
- Assist in the identification of primary hyperaldosteronism resulting from aldosterone-secreting adrenal adenoma.
- Assist in monitoring patients on mineralocorticoid therapy.
- Assist in the screening of the origin of essential, renal, or renovascular hypertension.
Factors that may alter the results of the study
- Drugs and other substances that may increase renin levels include albuterol, amiloride, azosemide, benazepril, bendroflumethiazide, captopril, chlorthalidone, cilazapril, desmopressin, diazoxide, dihydralazine, doxazosin, enalapril, endralazine, felodipine, fenoldopam, fosinopril, furosemide, hydralazine, hydrochlorothiazide, laxatives, lisinopril, lithium, methyclothiazide, metolazone, muzolimine, nicardipine, nifedipine, opiates, oral contraceptives, perindopril, ramipril, spironolactone, triamterene, and xipamide.
- Drugs and other substances that may decrease renin levels include acetylsalicylic acid, angiotensin, angiotensin II, atenolol, bopindolol, bucindolol, carbenoxolone, carvedilol, clonidine, cyclosporin A, glycyrrhiza, ibuprofen, indomethacin, levodopa, metoprolol, naproxen, nicardipine, NSAIDs, oral contraceptives, oxprenolol, propranolol, sulindac, and vasopressin.
- Upright body posture, stress, and strenuous exercise can increase renin levels.
- Diet can significantly affect results (e.g., low-sodium diets stimulate the release of renin).
- Hyperkalemia, acute increase in blood pressure, and increased blood volume may suppress renin secretion.
Potential Medical Diagnosis: Clinical Significance of Results
- Addison disease (related to hyponatremia, which stimulates production of renin)
- Bartter syndrome (related to hereditary defect in loop of Henle that affects sodium resorption; hyponatremia stimulates renin production)
- Cirrhosis (related to fluid buildup, which dilutes sodium concentration; hyponatremia is a strong stimulus for production of renin)
- Gastrointestinal disorders with electrolyte loss (related to hyponatremia, which stimulates production of renin)
- Heart failure (related to fluid buildup, which dilutes sodium concentration; hyponatremia is a strong stimulus for production of renin)
- Hepatitis (related to fluid buildup, which dilutes sodium concentration; hyponatremia is a strong stimulus for production of renin)
- Hypokalemia (related to decreased potassium levels, which stimulate renin production)
- Malignant hypertension (related to secondary hyperaldosteronism that constricts the blood vessels and results in hypertension)
- Nephritis (the kidneys can produce renin in response to inflammation or disease)
- Nephropathies with sodium or potassium wasting (related to hyponatremia, which stimulates production of renin)
- Pheochromocytoma (related to renin production in response to hypertension)
- Pregnancy (related to retention of fluid and hyponatremia that stimulates renin production; normal pregnancy is associated with changes in the balance between renin and angiotensin)
- Renin-producing kidney tumors
- Renovascular hypertension (related to decreased renal blood flow, which stimulates release of renin)
- Cushing syndrome (related to excessive production of glucocorticoids, which increase sodium levels and decrease potassium levels, inhibiting renin production)
- Primary hyperaldosteronism (related to aldosterone-secreting adrenal tumor; aldosterone inhibits renin production)
Before the Study: Planning and Implementation
Teaching the Patient What to Expect
- Inform the patient this test can assist in evaluating for high blood pressure.
- Explain that a blood sample is needed for the test. Inform the patient that multiple specimens may be required.
Potential Nursing Actions
- Verify adherence to ordered pretest instructions regarding diet and medications.
After the Study: Potential Nursing Actions
- Instruct the patient to resume usual medications, as directed by the HCP.
- Explain the importance of notifying the HCP of any signs and symptoms of dehydration or fluid overload related to abnormal renin levels or compromised sodium regulatory mechanisms. Fluid loss or dehydration is signaled by the thirst response. Decreased skin turgor, dry mouth, and multiple longitudinal furrows in the tongue are symptoms of dehydration. Fluid overload may be signaled by a loss of appetite and nausea. Excessive fluid also causes pitting edema: When firm pressure is placed on the skin over a bone (e.g., the ankle), the indentation will remain after 5 sec.
- Provide education on the importance of proper water balance. In the case of hard water, untreated tap water contains minerals such as calcium, magnesium, and iron. Water-softening systems replace these minerals with sodium, and therefore patients on a low-sodium diet should avoid drinking treated tap water and drink bottled water instead.
- Explain to patients with low sodium levels that the major source of dietary sodium is found in table salt. Many foods, such as milk and other dairy products, are also good sources of dietary sodium. Most other dietary sodium is available through the consumption of processed foods.
- Explain to patients on low-sodium diets to avoid beverages such as colas, ginger ale, sports drinks, lemon-lime sodas, and root beer. Many over-the-counter medications, including antacids, laxatives, analgesics, sedatives, and antitussives, contain significant amounts of sodium. A registered dietitian should be consulted before using salt substitutes.
- Explain that potassium is present in all plant and animal cells, making dietary replacement fairly simple to achieve.
Followup Evaluation and Desired Outcomes
- Recognizes the value of reading all food, beverage, and medicine labels to evaluate nutritional value.
- Understands that renin levels affect the regulation of fluid balance and electrolytes.
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