plasma renin activity


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Related to plasma renin activity: aldosterone

Plasma Renin Activity

 

Definition

Renin is an enzyme released by the kidney to help control the body's sodium-potassium balance, fluid volume, and blood pressure.

Purpose

Plasma renin activity (PRA), also called plasma renin assay, may be used to screen for high blood pressure (hypertension) of kidney origin, and may help plan treatment of essential hypertension, a genetic disease often aggravated by excess sodium intake. PRA is also used to further evaluate a diagnosis of excess aldosterone, a hormone secreted by the adrenal cortex, in a condition called Conn's syndrome.

Precautions

Patients taking diuretics, antihypertensives, vasodilators, oral contraceptives, and licorice should discontinue use of these substances for two to four weeks before the test. It should be noted that renin is increased in pregnancy and in diets with reduced salt intake. Also, since renin is affected by body position, as well as by diurnal (daily) variation, blood samples should be drawn in the morning, and the position of the patient (sitting or lying down) should be noted.

Description

When the kidneys release the enzyme renin in response to certain conditions (high blood potassium, low blood sodium, decreased blood volume), it is the first step in what is called the renin-angiotensin-aldosterone cycle. This cycle includes the conversion of angiotensinogen to angiotensin I, which in turn is converted to angiotensin II, in the lung. Angiotensin II is a powerful blood vessel constrictor, and its action stimulates the release of aldosterone from an area of the adrenal glands called the adrenal cortex. Together, angiotensin and aldosterone increase the blood volume, the blood pressure, and the blood sodium to re-establish the body's sodium-potassium and fluid volume balance. Primary aldosteronism, the symptoms of which include hypertension and low blood potassium (hypokalemia), is considered "low-renin aldosteronism."
Renin itself is not actually measured in the PRA test, because renin can be measured only with great difficulty even in research laboratories. In the most commonly used renin assay, the test actually determines, by a procedure called radioimmunoassay, the rate of angiotensin I generation per unit time, while the PRC (plasma renin concentration) measures the maximum renin effect.
Both the PRA and the PRC are extremely difficult to perform. Not only is renin itself unstable, but the patient's body position and the time of day affect the results. Also, the sample must be collected properly: drawn into a chilled syringe and collection tube, placed on ice, and sent to the performing laboratory immediately. Even if all these procedures are followed, results can vary significantly.
A determination of the PRA and a measurement of the plasma aldosterone level are used in the differential diagnosis of primary and secondary hyperaldosteronism. Patients with primary hyperaldosteronism (caused by an adrenal tumor that overproduces aldosterone) will have an increased aldosterone level with decreased renin activity. Conversely, patients with secondary hyperaldosteronism (caused by certain types of kidney disease) will have increased levels of renin.

Renin stimulation test

The renin stimulation test is performed to help diagnose and distinguish the two forms of hyperaldosteronism. With the patient having been on a low-salt diet and lying down for the test, a blood sample for PRA is obtained. The PRA is repeated with the patient still on the low salt diet but now standing upright. In cases of primary hyperaldosteronism, the blood volume is greatly expanded, and a change in position or reduced salt intake does not result in decreased kidney blood flow or decreased blood sodium. As a result, renin levels do not increase. However, in secondary hyperaldosteronism, blood sodium levels decrease with a lowered salt intake, and when the patient is standing upright, the kidney blood flow decreases as well. Consequently, renin levels do increase.

Captopril test

The captopril test is a screening test for hypertension of kidney origin (renovascular hypertension). For this test, a baseline PRA test is done first, then the patient receives an oral dose of captopril, which is an angiotensin-converting enzyme (ACE) inhibitor. Blood pressure measurements are taken at this time and again at 60 minutes when another PRA test is done. Patients with kidney-based hypertension demonstrate greater falls in blood pressure and increases in PRA after captopril administration than do those with essential hypertension. Consequently, the captopril test is an excellent screening procedure to determine the need for a more invasive radiographic evaluation such as renal arteriography.

Preparation

This test requires a blood sample. For the PRA, the patient should maintain a normal diet with a restricted amount of sodium (approximately 3 g per day) for three days before the test. It is recommended that the patient be fasting (nothing to eat or drink) from midnight the day of the test.

Risks

Risks for this test are minimal, but may include slight bleeding from the puncture site, fainting or feeling lightheaded after venipuncture, or hematoma (blood accumulating under the puncture site).

Normal results

Reference values for the PRA test are laboratory-specific and depend upon the kind of diet (sodium restricted or normal), the age of the patient, and the patient's posture at the time of the test. Values are also affected if renin has been stimulated or if the patient has received an ACE inhibitor, like captopril.

Abnormal results

Increased PRA levels are seen in essential hypertension (uncommon), malignant hypertension, and kidney-based (renovascular) hypertension. Renin-producing renal tumors, while rare, can also cause elevated levels, as can cirrhosis, low blood volume due to hemorrhage, and diminished adrenal function (Addison's disease). Decreased renin levels may indicate increased blood volume due to a high-sodium diet, salt-retaining steroids, primary aldosteronism, licorice ingestion syndrome, or essential hypertension with low renin levels.

Key terms

Aldosteronism — A disorder caused by excessive production of the hormone aldosterone, which is produced by a part of the adrenal glands called the adrenal cortex. Causes include a tumor of the adrenal gland (Conn's syndrome), or a disorder reducing the blood flow through the kidney. This leads to overproduction of renin and angiotensin, and in turn causes excessive aldosterone production. Symptoms include hypertension, impaired kidney function, thirst and muscle weakness.
Conn's syndrome — A disorder caused by excessive aldosterone secretion by a benign tumor of one of the adrenal glands. This results in malfunction of the body's salt and water balance and subsequently causes hypertension. Symptoms include thirst, muscle weakness, and excessive urination.

Resources

Books

Pagana, Kathleen Deska. Mosby's Manual of Diagnosticand Laboratory Tests. St. Louis: Mosby, Inc., 1998.

plas·ma re·nin ac·tiv·i·ty (PRA),

estimation of renin in plasma by measuring the rate of formation of angiotensin I or II.

plasma renin activity

the action of the enzyme renin (produced by the kidney), measured in plasma to aid in the diagnosis of adrenal disease associated with hypertension. The normal adult value in plasma is 0.2 to 4 ng/mL/hr, depending on salt intake and the time the patient is in an upright position before a renin activity test. An upright position raises production of renin, and a high salt intake lowers it.

plasma renin activity

A test for renovascular HTN in which peripheral venous blood obtained by catheterization from the renal vein is measured for the ability of the renin to convert angiotensinogen to angiotensin I ↑ in Addison's disease, renal HTN, 2º hypoaldosoteronism ↓ in Hyporeninemic hypoaldosteronism. See Hypertension, Renin.

plas·ma re·nin ac·ti·vi·ty

(PRA) (plaz'mă rē'nin ak-tiv'i-tē)
Estimation of renin in plasma by measurement of the rate of formation of angiotensin I or II.
References in periodicals archive ?
Calciumregulating hormones in essential hypertension: relation to plasma renin activity and sodium metabolism.
The same standard for plasma renin activity, for example, will yield a different absolute answer at every level when run at variable pH ranges.
Plasma renin activity by LC-MS/MS: development of a prototypical clinical assay reveals a subpopulation of human plasma samples with substantial peptidase activity.
SPP100, a novel renin inhibitor for treatment of hypertension, enhances renin system suppression by reducing plasma renin activity alone or in combination with ramipril in patients with diabetes(6)
In another experimental study, Ustundag et al (5) noted that the plasma renin activity levels were decreased with increased time period, whereas serum aldosterone levels were increased at days 3 and 12.
When patients were taken off SPP100, this was not associated with rebound increases in BP -- BP lowering persists for at least 2 weeks following withdrawal of SPP100, gradually returning towards baseline during this time -- Sustained BP lowering corresponds to suppression of Plasma Renin Activity (PRA) that is maintained following treatment withdrawal despite continued elevation of renin, suggesting a persistent effect of SPP100 treatment -- The sustained effect of SPP100 may be clinically beneficial, maintaining BP lowering in patients who miss occasional doses
As previously discussed, since hypersecretion of renin due to renal hypoperfusion is a primary event in the pathogenesis of RVHT, it is not surprising that patients with RVHT have been found to have elevated plasma renin activity (PRA).
Removal of the negative feedback of angiotensin II causes a 2-3 fold rise in plasma renin activity and consequent rise in angiotensin II plasma concentration in hypertensive patients.
Plasma renin activity (PRA) is a sensitive marker of mild volume depletion and can be increased in patients who are receiving inadequate doses of fludrocortisone, even if the patients have electrolyte concentrations within reference intervals (5).

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