Renin

Synonym/Acronym

plasma renin activity (PRA), angiotensinogenase.

Rationale

To assist in evaluating for a possible cause of hypertension.

Patient Preparation

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 for specimen collection (supine for infants or upright for children and adults) must be maintained for 15 to 30 min 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.

Normal Findings

Method: Liquid chromatography tandem mass spectrometry.

Age and Upright Position	Conventional Units	SI Units (Conventional Units × 1)
Newborn–12 mo	2–35 ng/mL/hr	2–35 mcg/L/hr
Normal sodium diet
Children (4–15 yr)	Equal to or less than 6 ng/mL/hr	Equal to or less than 6 mcg/L/hr
Greater than 15 yr–adult–older adult	0.2–4.3 ng/mL/hr	0.2–4.3 mcg/L/hr
Restricted sodium diet
18–39 yr	2.9–24 ng/mL/hr	2.9–24 mcg/L/hr
Greater than 40 yr	2.9–10.8 ng/mL/hr	2.9–10.8 mcg/L/hr
Aldosterone-Renin Ratio	Less than 25

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: Circulatory, endocrine, and urinary systems. Specify patient position [upright or supine] and exact source of specimen [peripheral versus arterial]. Venipuncture should be performed after the patient has been in the upright [sitting or standing] position for 15–30 min. 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”). Measurement of the aldosterone/renin ratio (ARR) from an adrenal venous sampling technique is the gold standard to distinguish between adrenal cortex adenoma (a benign unilateral hyperplasia that can be surgically corrected) and bilateral hyperplasia (treated medically with aldosterone antagonists). For additional information regarding the ARR, refer to the study titled “Aldosterone.”

Indications ⬆ ⬇

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.

Interfering Factors ⬆ ⬇

Drugs and other substances that may increase renin levels include albuterol, amiloride, azosemide, benazepril, bendroflumethiazide, captopril, chlorthalidone, cilazapril, desmopressin, diazoxide, dihydralazine, doxazosin, enalapril, 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, captopril, carbenoxolone, carvedilol, clonidine, cyclosporin A, furosimide, glycyrrhiza, indomethacin, labetolol, levodopa, metoprolol, naproxen, nicardipine, NSAIDs (ibuprofen, sulindac), oral contraceptives, oxprenolol, potassium, propranolol, reserpine, and vasopressin.
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 ⬆ ⬇

Increased In

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)

Decreased In

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)

Nursing Implications ⬆

Before the Study: Planning and Implementation

Teaching the Patient What to Expect

Discuss how 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: Implementation & Evaluation Potential Nursing Actions

Treatment Considerations

Resume the usual medications, as directed by the health-care provider (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, nausea, and pitting edema.
Interventions/actions include the following: 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.

Nutritional Considerations

Advise those with depleted sodium that the major source of dietary sodium is found in table salt, milk and other dairy products, and processed foods.
Advise those 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.

Clinical Judgement

Consider how to gain buy-in regarding reading food labels to help maintain a healthy sodium level.

Follow-Up 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.