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Establishing the diagnosis of renovascular hypertension

Establishing the diagnosis of renovascular hypertension
Literature review current through: Jan 2024.
This topic last updated: Jan 09, 2024.

INTRODUCTION — Renovascular disease is an important, potentially correctable cause of secondary hypertension. The frequency with which it occurs is variable. It accounts for less than 1 percent of cases of mild to moderate elevations in blood pressure [1]. By contrast, the prevalence is much higher in patients with acute (even if superimposed upon a preexisting elevation in blood pressure), severe, or refractory hypertension [2].

The indications for testing, methods of testing, and interpretation of diagnostic tests for renovascular disease will be reviewed here. The clinical features and clues to a diagnosis of renovascular hypertension, as well as the treatment of renovascular hypertension and ischemic nephropathy, are presented elsewhere:

(See "Evaluation of secondary hypertension", section on 'Clinical clues for renovascular hypertension'.)

(See "Treatment of unilateral atherosclerotic renal artery stenosis".)

(See "Treatment of bilateral atherosclerotic renal artery stenosis or stenosis to a solitary functioning kidney".)

(See "Treatment of fibromuscular dysplasia of the renal arteries".)

(See "Chronic kidney disease resulting from atherosclerotic renal artery stenosis".)

INDICATIONS FOR TESTING — Testing for renovascular disease is warranted in patients who fulfill all of the following criteria [2]:

The clinical findings suggest a cause of secondary hypertension rather than primary hypertension (formerly called "essential" hypertension).

The patient does not appear to have another cause of secondary hypertension such as primary kidney disease, primary aldosteronism, or pheochromocytoma. (See "Evaluation of secondary hypertension", section on 'Clues for other major forms of secondary hypertension'.)

Renal revascularization or another intervention would be planned or considered if a significant stenotic lesion is found.

There are a variety of clinical findings that increase the likelihood that hypertension is at least partly due to renovascular disease or another cause of secondary hypertension (table 1). These findings include severe and/or resistant hypertension, an acute rise in blood pressure over a previously stable value, and young onset hypertension with a negative family history. In addition, there are other findings that are more specific for renovascular disease. These include an otherwise unexplained acute and sustained rise in serum creatinine of more than 30 percent after initiating a renin-angiotensin system inhibitor (eg, angiotensin-converting enzyme [ACE] inhibitor), moderate to severe hypertension in a patient with diffuse atherosclerosis, renal asymmetry (eg, a unilateral small kidney) that cannot be explained by another reason, or recurrent episodes of flash pulmonary edema (table 1). (See "Evaluation of secondary hypertension", section on 'Clinical clues for renovascular hypertension'.)

In addition to estimating the likelihood that a patient has renovascular disease, other considerations should contribute to the decision of whether or not to pursue an evaluation for renal artery stenosis:

Antihypertensive drugs can effectively control the blood pressure in many patients with renovascular hypertension. Prospective, randomized treatment trials for individuals with moderate renovascular disease suggest that little additional benefit is gained from renal revascularization if blood pressure is well controlled and kidney function remains stable. (See "Treatment of unilateral atherosclerotic renal artery stenosis".)

Other than an otherwise unexplained acute and persistent elevation in blood pressure above a previously stable baseline, there are no routine clinical, laboratory, or radiological features that consistently predict who will benefit from correction of the renovascular disease [3]. Lateralization of renal vein renin measurements does predict a reduction in blood pressure after revascularization, but this invasive test also produces many false negative results. (See 'Renal vein renin measurements' below.)

Testing for renovascular disease is associated with potential risks, particularly in patients with impaired kidney function who undergo digital subtraction angiography. (See 'Diagnostic test options' below and "Prevention of contrast-associated acute kidney injury related to angiography" and "Prevention of contrast-induced acute kidney injury associated with computed tomography" and "Nephrogenic systemic fibrosis/nephrogenic fibrosing dermopathy in advanced kidney disease".)

Procedures undertaken to correct renal artery stenosis can be associated with morbidity and mortality, particularly in patients with underlying chronic kidney disease. (See "Treatment of unilateral atherosclerotic renal artery stenosis", section on 'Procedural complications' and "Treatment of unilateral atherosclerotic renal artery stenosis", section on 'Surgery' and "Treatment of bilateral atherosclerotic renal artery stenosis or stenosis to a solitary functioning kidney", section on 'Procedural complications' and "Treatment of bilateral atherosclerotic renal artery stenosis or stenosis to a solitary functioning kidney", section on 'Surgery'.)

Because of the potential for harm from invasive procedures, we test only those patients who are thought to have a high likelihood of benefiting from the procedure. The following scenarios identify such patients:

A short duration (weeks or months) of blood pressure elevation prior to the diagnosis of renovascular disease, even if the blood pressure can be controlled with drug therapy, since this is the strongest clinical predictor of a fall in blood pressure after renal revascularization [4].

Failure of optimal medical therapy to control the blood pressure in someone who has, based upon clinical clues, a high likelihood of having renovascular disease. (See "Evaluation of secondary hypertension", section on 'Clinical clues for renovascular hypertension'.)

Intolerance to optimal medical therapy, including a clinically significant rise in serum creatinine after initiation of a renin-angiotensin system inhibitor.

Progressive kidney function impairment that is thought be a consequence of bilateral renovascular disease or unilateral stenosis affecting a solitary functioning kidney. (See "Chronic kidney disease resulting from atherosclerotic renal artery stenosis".)

Suspected fibromuscular disease in a young person in an attempt to limit the need for life-long antihypertensive therapy. (See "Treatment of fibromuscular dysplasia of the renal arteries", section on 'Angioplasty versus surgery'.)

Recurrent flash pulmonary edema and/or refractory heart failure. (See "Treatment of acute decompensated heart failure: General considerations", section on 'Renovascular hypertension'.)

Testing should not be performed in patients who have a moderate or low likelihood of having clinically significant renovascular disease or who respond well to medical therapy. The existing randomized trials comparing percutaneous revascularization with medical therapy primarily consisted of patients with moderate and low likelihood of clinically important renovascular disease and, during three to five years of follow-up, showed no evidence of benefit from adding revascularization to optimal medical therapy. (See "Treatment of unilateral atherosclerotic renal artery stenosis".)

DIAGNOSTIC TEST OPTIONS — We generally agree with the 2019 American College of Cardiology/American Heart Association (ACC/AHA) guidelines on peripheral artery disease [5], 2014 consensus statement from the Society of Cardiovascular Angiography and Interventions (SCAI), and 2017 ACC/AHA hypertension guidelines related to appropriate indications for renal revascularization [6,7]. Testing for renal artery stenosis is indicated if a corrective procedure would be performed if clinically significant renovascular disease were detected. (See 'Indications for testing' above.)

Testing options — The gold standard for diagnosing renal artery stenosis is renal arteriography (image 1). However, a variety of less invasive tests has been evaluated for testing purposes [1,2]. The following noninvasive tests are reasonable alternatives for initial testing [8]:

Duplex Doppler ultrasonography

Computed tomographic angiography (CTA)

Magnetic resonance angiography (MRA)

The choice of test should be based upon institutional expertise and patient factors (see 'Selecting a diagnostic test' below). If the noninvasive test is inconclusive and the clinical suspicion remains high, further testing, and/or conventional renal arteriography is recommended.

Captopril renal scintigraphy (renography), selective renal vein renin measurements, and plasma renin activity (in isolation or after captopril administration) are not as useful as initial diagnostic tests for renal artery stenosis, although renography is useful to determine the relative function of each kidney. (See 'Tests of limited utility, but occasionally performed' below.)

Duplex Doppler ultrasonography — Duplex Doppler ultrasonography primarily provides functional assessment of the renal arteries, as well as some anatomic information. Direct visualization of the main renal arteries (B-mode imaging) is combined with measurement (via Doppler) of a variety of hemodynamic factors. Stenotic lesions can be detected by comparing the systolic flow velocity in the renal artery to that in the aorta since the velocity of flow increases as an artery narrows; end-diastolic velocity also may be increased distal to a stenotic lesion.

Duplex Doppler ultrasonography can detect both unilateral and bilateral disease. It is relatively inexpensive and suitable for serial measurements to determine disease progression. This modality can also be used to detect recurrent stenosis in patients previously treated with angioplasty or surgery.

A meta-analysis of 88 studies involving 9974 arteries and 8147 patients assessed the ability of the various duplex ultrasonography parameters to detect renal artery stenosis [9]. Of these parameters, peak systolic velocity, with a sensitivity and specificity of 85 and 92 percent, respectively, was more accurate than the renal-aortic ratio and acceleration index. The positive predictive value was 84 percent, and the false positive rate was 8 percent.

There are, however, two important disadvantages of duplex Doppler ultrasonography:

It is time consuming (taking up to two hours to perform).

It is technically difficult (particularly in large patients), has a substantial learning curve, and is operator dependent.

As with many diagnostic procedures, a positive test is more informative than a negative test.

Resistive index — When added to duplex Doppler ultrasonography, calculation of the renal resistive index ([peak systolic velocity - end-diastolic velocity] divided by peak systolic velocity) may, in the hands of experienced operators, improve the ability to predict the outcome after revascularization. In general, a higher resistive index is associated with a greater degree of intrinsic kidney damage (ie, likely irreversible small vessel injury) and, therefore, a diminished predicted benefit from revascularization.

The utility of the resistive index was evaluated in a study of almost 6000 patients with hypertension and clinical features suggestive of atherosclerotic renovascular disease [10]. The following findings were noted in the 131 patients who had renal artery stenosis and underwent technically successful angioplasty, primarily without stent placement:

The outcomes were poor among the 35 patients with a resistive index above 80. Kidney function declined during follow-up in 80 percent of these patients, nearly one-half became dialysis dependent, and only one experienced a blood pressure reduction of ≥10 mmHg. Thus, a high resistance index may indicate irreversible intrarenal vascular disease or arteriosclerosis [11].

The outcomes were better among the 96 patients with a resistive index less than 80. There was a significant fall in blood pressure in 94 percent, while kidney function worsened in only 3 percent. These patients had significantly better baseline kidney function than those with a higher resistance index (creatinine clearance 68 versus 33 mL/min) and were less likely to have a history of severe atherosclerosis (54 versus 83 percent).

Although similar findings have been found in some studies [12], this marked difference in outcomes according to the resistive index was not replicated in other studies [13-15]. In addition, determination of the resistive index is operator dependent and can be obscured by patient factors such as obesity. Thus, it is not, by itself, a broadly reliable parameter for predicting the outcome after revascularization.

Spiral CT scan with CT angiography — A spiral (helical) computed tomography (CT) scan with intravenous contrast injection (called CT angiography, or CTA) is a highly accurate noninvasive diagnostic test for imaging renovascular disease due to atherosclerosis but less so for fibromuscular disease (image 2). (See "Principles of computed tomography of the chest".)

CT angiography combines the diagnostic accuracy of arteriography with the low risk of intravenous digital subtraction angiography. Multidetector, spiral CTA continues to evolve technically and has been reported to provide excellent sensitivity (96 percent) and specificity (97 percent) in small groups of patients [14-18].

The performance of CTA was less favorable in a larger series of 356 hypertensive patients, of whom 72 patients (20 percent) had some degree of renal artery stenosis (defined as a 50 percent or greater stenosis detected by digital subtraction angiography) [19]. The sensitivity and specificity of CTA were 64 and 92 percent, respectively. However, the poor sensitivity of CTA in this study was probably due to the high proportion of patients who had fibromuscular dysplasia (36 percent of those with renal artery stenosis) since fibromuscular disease usually involves distal arterial segments that are more difficult to image. (See 'Noninvasive imaging is less reliable in fibromuscular dysplasia' below.)

Rapid developments in CT imaging with improved tissue reconstruction, multidetector slice acquisition, and higher resolution with less contrast exposure continue to improve the value of CT angiography as a diagnostic tool for renovascular disease.

Magnetic resonance angiography — Contrast-enhanced magnetic resonance angiography (MRA) can provide excellent vascular imaging (image 3). Type 2 gadolinium agents, which are generally not associated with nephrogenic systemic fibrosis, are widely used today. Thus, concerns about gadolinium-associated complications including nephrogenic systemic fibrosis are greatly reduced. The level of glomerular filtration rate below which MRA is generally avoided is discussed below. (See 'Patients with kidney function impairment' below and "Nephrogenic systemic fibrosis/nephrogenic fibrosing dermopathy in advanced kidney disease".)

MRA is a highly sensitive technique for detecting proximal renal artery stenosis, as noted by the following studies:

In a series of 37 patients with hypertension who underwent both MRA and digital subtraction arteriography, 12 had renal artery stenosis of at least 50 percent [20]. Using arteriography as the gold standard, MRA had a sensitivity of 100 percent and specificity of 96 percent (one false positive) for the detection of stenosis of the main renal arteries. However, MRA missed stenosis in 9 of 12 accessory renal arteries.

Similar findings were noted in another report of 30 patients: sensitivity of 100 percent and specificity of 71 percent for proximal renal artery stenoses of more than 50 or 75 percent occlusion [21].

Technical improvements in MRA, including imaging without the use of gadolinium-based contrast, have enhanced the detection of significant renal artery disease [22,23]. As an example, the use of breath-hold MRA with paramagnetic contrast material such as gadopentetate dimeglumine substantially improves the ability to visualize some (but not all) accessory arteries [19], while phase-contrast MRA produces results similar to digital subtraction angiography [24]. In one report of 87 renal arteries, 20 of which had a stenosis, the sensitivity and specificity of breath-hold MRA for renal artery stenosis were 100 and 98 percent, respectively [25].

Noninvasive imaging is less reliable in fibromuscular dysplasia — The risk of a false negative result from noninvasive imaging is much more likely to occur in patients with stenotic lesions that involve the intrarenal portion of the renal artery. Disease in these distal arterial segments is most common in patients with fibromuscular dysplasia. Sensitivities of only 22 to 28 percent have been noted with MR and CT angiography in this setting [19,26]. The preferred approach in these patients is discussed separately. (See "Clinical manifestations and diagnosis of fibromuscular dysplasia", section on 'Choice of diagnostic imaging'.)

Tests of limited utility, but occasionally performed — Other noninvasive tests, such as peripheral plasma renin activity (PRA), stimulated PRA, and the captopril renogram are no longer considered suitable for initial testing patients with suspected renovascular disease because of their poor sensitivity and specificity [8]. However, a captopril renogram may help assess the hemodynamic significance of a stenotic lesion. (See 'Interpreting the results of diagnostic tests' below.)

Plasma renin activity — Peripheral venous PRA is elevated in only 50 to 80 percent of patients with renovascular hypertension [27]. This may partly reflect the observation that, in experimental models, activation of the renin-angiotensin system can be transient in the development of renovascular hypertension [28]. In clinical settings, levels of PRA may be suppressed by a high dietary sodium intake, bilateral renal arterial disease, volume expansion related to intrinsic kidney disease, and various antihypertensive drugs [29]. It has limited value for the diagnosis of renovascular hypertension.

The predictive value of the PRA can be increased by measuring the rise in PRA one hour after the administration of 25 to 50 mg of captopril, a rapidly acting angiotensin-converting enzyme (ACE) inhibitor [27,30]. Patients with renal artery stenosis have an exaggerated increase in the PRA as compared with normal individuals, perhaps due to removal of the normal suppressive effect of high angiotensin II levels on renin secretion in the stenotic kidney.

Measurement of renal vein renin levels does allow more precise estimation of a specific vascular lesion as the driver (or "pressor kidney") in renovascular hypertension. We use this measurement if considering nephrectomy for blood pressure control, which is infrequently performed [31].

Captopril renogram — Radionuclide imaging provides a functional test allowing the comparison of blood flow and filtration between two kidneys. Markers of glomerular filtration, such as DTPA, or compounds that are secreted by the proximal tubule, such as hippurate and MAG3, have been used as radionuclides in renography. MAG3 may be more reliable in patients with kidney function impairment [32]. Due to various limitations, captopril renography is not broadly helpful in diagnosing renal artery stenosis.

Nonstimulated renal scans have a false negative rate of 20 to 25 percent and are therefore of limited efficacy as a diagnostic test for renovascular disease [33]. The predictive value of radioisotope scanning can be increased by administration of oral captopril (25 to 50 mg) one hour before the isotope is injected [34]. The efficacy of this test is based upon the expected ACE inhibitor-induced decline in glomerular filtration rate (GFR) in the stenotic kidney, often accompanied by an increase in GFR in the contralateral kidney due to removal of angiotensin II-mediated vasoconstriction. The net effect is that the difference between the two kidneys is enhanced. (See "Renal effects of ACE inhibitors in hypertension".)

The sensitivity and specificity of the ACE inhibitor scan vary substantially in different studies [33-37], and have limited interobserver agreement and a poor correlation with the benefit obtained from angioplasty [36,37]. An additional problem is the high prevalence of baseline asymmetry of renal blood flow, particularly in patients with a reduced glomerular filtration rate. In a study of 148 patients with primary hypertension, for example, one-half of patients had a greater than 25 percent difference in renal blood flow between the two kidneys [38].

As a result of these limitations, we use radionuclide renography primarily to determine the relative function of each kidney. As an example, some patients with uncontrolled hypertension who have unilateral renovascular occlusion benefit from therapeutic nephrectomy [31]. This is an acceptable therapeutic strategy, particularly when the affected kidney accounts for less than 15 percent of the total GFR [31].

Renal vein renin measurements — Renin secretion should be increased in the stenotic kidney (as evidenced by a renal vein renin that is ≥1.5 times the value from the contralateral kidney), and suppressed in the contralateral kidney (as evidenced by the renal vein renin from that kidney being similar to arterial renin, which is estimated from a blood sample obtained from the infrarenal inferior vena cava) [32]. This large discrepancy in renin secretion between the two kidneys is present in less than 10 percent of normal individuals [32]. Thus, the presence of highly discrepant (or lateralizing) renal renin values should indicate the presence of physiologically significant renal artery stenosis. The accuracy of these measurements may be enhanced by the prior administration of an ACE inhibitor and/or diuretics, which increase renin secretion on the affected side.

However, the use of renal vein renin measurements to diagnose clinically significant renovascular disease produces many false negative and occasional false positive results [35,39]. Although more than 90 percent of patients with unilateral renal artery stenosis and lateralizing renin values will have a favorable blood pressure response to angioplasty or surgery [40], so will approximately 50 percent of patients with nonlateralizing renin values. The benefit of angioplasty observed in patients with nonlateralizing renin values may be due to suppression of renin secretion resulting from volume expansion, which is commonly used to reduce the risks of contrast nephrotoxicity [41].

Thus, renal vein renins have a limited role in estimating the physiologic significance of a stenotic lesion. Exceptions may include patients with bilateral renal artery stenosis in whom renal vein renin measurements can be used to determine which side contributes more to the hypertension or in patients considered for nephrectomy of a pressor kidney [31,32,42].

SELECTING A DIAGNOSTIC TEST — Testing for renal artery stenosis is only indicated if a corrective procedure would be performed if clinically significant renovascular disease were detected [2]. Potential indications for testing are discussed above. (See 'Indications for testing' above and "Evaluation of secondary hypertension".)

Even though they are noninvasive, a spiral CT scan, MR angiography, and duplex ultrasonography are not useful for testing a population at low risk for renovascular hypertension [43]. As an example, a test with a sensitivity and specificity of 95 percent will have a positive predictive value of only 16 percent if the prevalence of disease is 1 percent [19].

There is no sufficiently accurate, noninvasive radiologic or serologic diagnostic test that, if negative, will completely exclude the presence of renal artery stenosis [19,24]. Each test is associated with strengths and weaknesses. (See 'Diagnostic test options' above.)

If a decision is made to evaluate for renovascular disease, the test of choice depends upon the local availability and clinical expertise with each technique and the presence or absence of kidney function impairment, because radiocontrast media and older gadolinium-based agents are potentially harmful in patients with stage 4 or 5 chronic kidney disease (ie, a glomerular filtration rate less than 30 mL/min per 1.73 m2).

Patients without kidney function impairment — Duplex Doppler, CTA, and MRA all provide minimally invasive options for diagnostic evaluation prior to intra-arterial angiography in patients with normal or near-normal kidney function. They are most accurate for proximal disease. In addition to diagnosing renal artery stenosis, these tests can identify anatomic abnormalities of the kidneys, aortic disease (such as abdominal aortic aneurysm), and whether the stenosis is unilateral or bilateral.

A negative Doppler study does not exclude renal artery stenosis. Thus, digital subtraction arteriography should be performed when noninvasive testing is inconclusive. If the arteriogram is positive, endovascular revascularization, often with primary renal artery stenting, can be performed during the same procedure.

Patients with kidney function impairment — In patients with kidney function impairment, an evaluation for renovascular disease should be considered in those who are likely to have chronic ischemic kidney disease. In addition to hypertension, which is often difficult to control, patients with chronic ischemic kidney disease tend to present with a characteristic (but not diagnostic) constellation of findings (see "Chronic kidney disease resulting from atherosclerotic renal artery stenosis"):

Unexplained progressive kidney failure, with occasional acute deterioration or even anuria if the one functional artery progresses to total occlusion

A bland urine sediment with few cells or casts or mild to moderate proteinuria

A unilateral small kidney, which is associated with the presence of large vessel occlusive disease in 75 percent of cases

The optimal approach to such patients is uncertain, although some will have recovery of kidney function or slowing of kidney function decline after successful revascularization [44-46]. The primary indications for testing in patients suspected of having chronic ischemic kidney disease are:

Progressive decline in kidney function

Recurrent episodes of flash pulmonary edema

Uncontrolled hypertension

Both noninvasive testing and angiography carry risk in these individuals, including contrast-induced acute kidney injury, nephrogenic systemic fibrosis (due to gadolinium if magnetic resonance angiography is used), and atheroembolism with conventional arteriography [47]. (See "Nephrogenic systemic fibrosis/nephrogenic fibrosing dermopathy in advanced kidney disease" and "Contrast-associated and contrast-induced acute kidney injury: Clinical features, diagnosis, and management" and "Clinical presentation, evaluation, and treatment of renal atheroemboli".)

We suggest the following approach to the evaluation of renovascular disease in patients with severe kidney function impairment (ie, estimated glomerular filtration rate [eGFR] less than 30 mL/min/1.73m2):

If technical expertise is available, duplex Doppler ultrasonography is the preferred initial noninvasive diagnostic test since both gadolinium and radiocontrast media exposure are avoided [9].

If expertise with Doppler ultrasonography is unavailable, we prefer spiral CT scan with CT angiography, despite the modest risk of radiocontrast nephropathy. In such patients, preventive measures for contrast nephrotoxicity should be used. (See "Prevention of contrast-induced acute kidney injury associated with computed tomography".)

In the past, MRA had been avoided in most patients with impaired kidney function due to the risk of nephrogenic systemic fibrosis with type 1 gadolinium agents. However, type 2 gadolinium agents are primarily used today and are generally not associated with nephrogenic systemic fibrosis. Nevertheless, gadolinium-based imaging is avoided in many patients with an eGFR less than 30 mL/min/1.732. (See "Patient evaluation before gadolinium contrast administration for magnetic resonance imaging", section on 'Approach to preventing nephrogenic systemic fibrosis' and "Nephrogenic systemic fibrosis/nephrogenic fibrosing dermopathy in advanced kidney disease", section on 'Prevention'.)

INTERPRETING THE RESULTS OF DIAGNOSTIC TESTS — Testing for renovascular disease is only recommended when the plan is to intervene if a significant stenotic lesion is found. Potential indications for testing are presented above. (See 'Indications for testing' above.)

With duplex Doppler ultrasonography, a peak systolic velocity above 200 cm/sec suggests a stenosis of greater than 60 percent, although some studies indicate that a peak systolic velocity above 300 cm/sec represents a hemodynamically important threshold [48]. With computed tomography and magnetic resonance angiography, a stenosis greater than 75 percent in one or both renal arteries or a 50 percent stenosis with poststenotic dilatation suggests that the patient may have renovascular hypertension.

However, quantifying the actual degree of stenosis can be difficult. Experimental studies indicate that luminal occlusion less than 60 percent rarely produces any measurable hemodynamic effects, including a fall in pressure or blood flow across the lesion. Human studies using translesional pressure measurements have shown that a blood pressure gradient of at least 10 to 20 percent across the stenosis is required to detect stimulation of renin release [49]. The corollary of this finding is that revascularization is not warranted if no translesional gradient is detected.

Incidental lesions — Patients are often incidentally discovered to have atherosclerotic renal artery stenosis. Radiographic evaluation for peripheral artery disease or coronary disease often reveals that renal arterial lesions are present in patients who are not hypertensive [50,51]. Patients with incidentally discovered atherosclerotic renal artery stenosis do not require therapy directed at the renal vasculature, since there is evidence that renal artery revascularization in such patients does not improve blood pressure or other outcomes in this setting [52]. The frequency with which this occurs is discussed in detail elsewhere. (See "Chronic kidney disease resulting from atherosclerotic renal artery stenosis".)

SOCIETY GUIDELINE LINKS — Links to society and government-sponsored guidelines from selected countries and regions around the world are provided separately. (See "Society guideline links: Hypertension in adults".)

INFORMATION FOR PATIENTS — UpToDate offers two types of patient education materials, "The Basics" and "Beyond the Basics." The Basics patient education pieces are written in plain language, at the 5th to 6th grade reading level, and they answer the four or five key questions a patient might have about a given condition. These articles are best for patients who want a general overview and who prefer short, easy-to-read materials. Beyond the Basics patient education pieces are longer, more sophisticated, and more detailed. These articles are written at the 10th to 12th grade reading level and are best for patients who want in-depth information and are comfortable with some medical jargon.

Here are the patient education articles that are relevant to this topic. We encourage you to print or e-mail these topics to your patients. (You can also locate patient education articles on a variety of subjects by searching on "patient info" and the keyword(s) of interest.)

Basics topics (see "Patient education: Renovascular hypertension (The Basics)")

Beyond the Basics topics (see "Patient education: High blood pressure in adults (Beyond the Basics)" and "Patient education: High blood pressure treatment in adults (Beyond the Basics)" and "Patient education: High blood pressure, diet, and weight (Beyond the Basics)")

SUMMARY AND RECOMMENDATIONS

Because of the potential for harm from invasive procedures, we test only those patients who are thought to have a high likelihood of benefiting from the procedure. The following scenarios identify such patients (see 'Indications for testing' above):

A short duration (weeks or months) of blood pressure elevation prior to the diagnosis of renovascular disease, since this is the strongest clinical predictor of a fall in blood pressure after renal revascularization

Failure of optimal medical therapy to control the blood pressure in someone who has, based upon clinical clues, a high likelihood of having renovascular disease

Intolerance to optimal medical therapy, including a clinically significant rise in serum creatinine after initiation of a renin-angiotensin system inhibitor

Progressive kidney function impairment that is thought be a consequence of bilateral renovascular disease or unilateral stenosis affecting a solitary functioning kidney

Suspected fibromuscular disease in a young person in an attempt to limit the need for life-long antihypertensive therapy

Recurrent flash pulmonary edema and/or refractory heart failure

Testing should not be performed in patients who have a moderate or low likelihood of having clinically significant renovascular disease or who respond well to medical therapy. (See 'Indications for testing' above.)

Reasonable alternatives for initial testing include duplex Doppler ultrasonography, computed tomographic angiography (CTA), and magnetic resonance angiography (MRA). (See 'Testing options' above and 'Duplex Doppler ultrasonography' above and 'Spiral CT scan with CT angiography' above and 'Magnetic resonance angiography' above.)

The risk of a false negative result from noninvasive imaging is much more likely to occur in patients with stenotic lesions that involve the intrarenal portion of the renal artery, which are common in patients with fibromuscular dysplasia. (See 'Noninvasive imaging is less reliable in fibromuscular dysplasia' above.)

Captopril renal scintigraphy (renography), selective renal vein renin measurements, and plasma renin activity (in isolation or after captopril administration) are not as useful as initial diagnostic tests for renal artery stenosis, although each may have confirmatory roles. (See 'Tests of limited utility, but occasionally performed' above.)

The test of choice depends upon the local availability and clinical expertise with each technique and the presence or absence of severe kidney function impairment. There is no sufficiently accurate, noninvasive radiologic or serologic diagnostic test that, if negative, will completely exclude the presence of renal artery stenosis. Thus, if the noninvasive test is inconclusive and the clinical suspicion remains high, conventional renal arteriography is recommended. (See 'Selecting a diagnostic test' above.)

In patients without kidney function impairment, duplex Doppler, CTA, and MRA all provide minimally invasive options for diagnostic evaluation prior to intra-arterial angiography. (See 'Patients without kidney function impairment' above.)

In patients with severe kidney function impairment (ie, estimated glomerular filtration rate [eGFR] less than 30 mL/min/1.73m2), both noninvasive testing and angiography carry risk, including contrast-induced acute kidney injury, nephrogenic systemic fibrosis (due to gadolinium if MRA is used), and atheroembolism with conventional arteriography. If technical expertise is available, duplex Doppler ultrasonography is the preferred initial noninvasive diagnostic test. If expertise with Doppler ultrasonography is unavailable, CTA or MRA may be used. (See 'Patients with kidney function impairment' above.)

With duplex Doppler ultrasonography, a peak systolic velocity above 200 cm/sec suggests a stenosis of greater than 60 percent, although some studies indicate that a peak systolic velocity above 300 cm/sec represents a hemodynamically important threshold. With CTA and MRA, a stenosis greater than 75 percent in one or both renal arteries or a 50 percent stenosis with poststenotic dilatation suggests that the patient may have renovascular hypertension. (See 'Interpreting the results of diagnostic tests' above.)

  1. Dworkin LD, Cooper CJ. Clinical practice. Renal-artery stenosis. N Engl J Med 2009; 361:1972.
  2. Textor SC, Lerman L. Renovascular hypertension and ischemic nephropathy. Am J Hypertens 2010; 23:1159.
  3. Ronden RA, Houben AJ, Kessels AG, et al. Predictors of clinical outcome after stent placement in atherosclerotic renal artery stenosis: a systematic review and meta-analysis of prospective studies. J Hypertens 2010; 28:2370.
  4. Hughes JS, Dove HG, Gifford RW Jr, Feinstein AR. Duration of blood pressure elevation in accurately predicting surgical cure of renovascular hypertension. Am Heart J 1981; 101:408.
  5. Bailey SR, Beckman JA, Dao TD, et al. ACC/AHA/SCAI/SIR/SVM 2018 Appropriate Use Criteria for Peripheral Artery Intervention: A Report of the American College of Cardiology Appropriate Use Criteria Task Force, American Heart Association, Society for Cardiovascular Angiography and Interventions, Society of Interventional Radiology, and Society for Vascular Medicine. J Am Coll Cardiol 2019; 73:214.
  6. 2011 WRITING GROUP MEMBERS, 2005 WRITING COMMITTEE MEMBERS, ACCF/AHA TASK FORCE MEMBERS. 2011 ACCF/AHA Focused Update of the Guideline for the Management of patients with peripheral artery disease (Updating the 2005 Guideline): a report of the American College of Cardiology Foundation/American Heart Association Task Force on practice guidelines. Circulation 2011; 124:2020.
  7. Whelton PK, Carey RM, Aronow WS, et al. 2017 ACC/AHA/AAPA/ABC/ACPM/AGS/APhA/ASH/ASPC/NMA/PCNA Guideline for the Prevention, Detection, Evaluation, and Management of High Blood Pressure in Adults: A Report of the American College of Cardiology/American Heart Association Task Force on Clinical Practice Guidelines. J Am Coll Cardiol 2018; 71:e127.
  8. Hirsch AT, Haskal ZJ, Hertzer NR, et al. ACC/AHA 2005 Practice Guidelines for the management of patients with peripheral arterial disease (lower extremity, renal, mesenteric, and abdominal aortic): a collaborative report from the American Association for Vascular Surgery/Society for Vascular Surgery, Society for Cardiovascular Angiography and Interventions, Society for Vascular Medicine and Biology, Society of Interventional Radiology, and the ACC/AHA Task Force on Practice Guidelines (Writing Committee to Develop Guidelines for the Management of Patients With Peripheral Arterial Disease): endorsed by the American Association of Cardiovascular and Pulmonary Rehabilitation; National Heart, Lung, and Blood Institute; Society for Vascular Nursing; TransAtlantic Inter-Society Consensus; and Vascular Disease Foundation. Circulation 2006; 113:e463.
  9. Williams GJ, Macaskill P, Chan SF, et al. Comparative accuracy of renal duplex sonographic parameters in the diagnosis of renal artery stenosis: paired and unpaired analysis. AJR Am J Roentgenol 2007; 188:798.
  10. Radermacher J, Chavan A, Bleck J, et al. Use of Doppler ultrasonography to predict the outcome of therapy for renal-artery stenosis. N Engl J Med 2001; 344:410.
  11. Ikee R, Kobayashi S, Hemmi N, et al. Correlation between the resistive index by Doppler ultrasound and kidney function and histology. Am J Kidney Dis 2005; 46:603.
  12. Santos S, Leite LR, Tse TS, et al. [Renal resistance index predicting outcome of renal revascularization for renovascular hypertension]. Arq Bras Cardiol 2010; 94:452.
  13. Krumme B, Hollenbeck M. Doppler sonography in renal artery stenosis--does the Resistive Index predict the success of intervention? Nephrol Dial Transplant 2007; 22:692.
  14. Crutchley TA, Pearce JD, Craven TE, et al. Clinical utility of the resistive index in atherosclerotic renovascular disease. J Vasc Surg 2009; 49:148.
  15. Zeller T, Müller C, Frank U, et al. Stent angioplasty of severe atherosclerotic ostial renal artery stenosis in patients with diabetes mellitus and nephrosclerosis. Catheter Cardiovasc Interv 2003; 58:510.
  16. Echevarría JJ, Miguélez JL, López-Romero S, et al. [Arteriographic correlation in 30 patients with renal vascular disease diagnosed with multislice CT]. Radiologia 2008; 50:393.
  17. Glockner JF, Vrtiska TJ. Renal MR and CT angiography: current concepts. Abdom Imaging 2007; 32:407.
  18. Olbricht CJ, Paul K, Prokop M, et al. Minimally invasive diagnosis of renal artery stenosis by spiral computed tomography angiography. Kidney Int 1995; 48:1332.
  19. Vasbinder GB, Nelemans PJ, Kessels AG, et al. Accuracy of computed tomographic angiography and magnetic resonance angiography for diagnosing renal artery stenosis. Ann Intern Med 2004; 141:674.
  20. Postma CT, Joosten FB, Rosenbusch G, Thien T. Magnetic resonance angiography has a high reliability in the detection of renal artery stenosis. Am J Hypertens 1997; 10:957.
  21. Rieumont MJ, Kaufman JA, Geller SC, et al. Evaluation of renal artery stenosis with dynamic gadolinium-enhanced MR angiography. AJR Am J Roentgenol 1997; 169:39.
  22. Schoenberg SO, Rieger J, Johannson LO, et al. Diagnosis of renal artery stenosis with magnetic resonance angiography: update 2003. Nephrol Dial Transplant 2003; 18:1252.
  23. Schoenberg SO, Knopp MV, Londy F, et al. Morphologic and functional magnetic resonance imaging of renal artery stenosis: a multireader tricenter study. J Am Soc Nephrol 2002; 13:158.
  24. Textor SC. Pitfalls in imaging for renal artery stenosis. Ann Intern Med 2004; 141:730.
  25. Thornton MJ, Thornton F, O'Callaghan J, et al. Evaluation of dynamic gadolinium-enhanced breath-hold MR angiography in the diagnosis of renal artery stenosis. AJR Am J Roentgenol 1999; 173:1279.
  26. Slovut DP, Olin JW. Fibromuscular dysplasia. N Engl J Med 2004; 350:1862.
  27. Wilcox CS. Use of angiotensin-converting-enzyme inhibitors for diagnosing renovascular hypertension. Kidney Int 1993; 44:1379.
  28. Lerman LO, Nath KA, Rodriguez-Porcel M, et al. Increased oxidative stress in experimental renovascular hypertension. Hypertension 2001; 37:541.
  29. Townsend SC. Renovascular hypertension and ischemic nephropathy. In: Brenner and Rector's The Kidney, 10th ed, Skorecki K, Chertow GM, Marsden PA, Taal MW, Yu ASL (Eds), Elsevier, Philadelphia 2016. Vol 2, p.1567.
  30. Svetkey LP, Kadir S, Dunnick NR, et al. Similar prevalence of renovascular hypertension in selected blacks and whites. Hypertension 1991; 17:678.
  31. Kane GC, Textor SC, Schirger A, Garovic VD. Revisiting the role of nephrectomy for advanced renovascular disease. Am J Med 2003; 114:729.
  32. Derkx FH, Schalekamp MA. Renal artery stenosis and hypertension. Lancet 1994; 344:237.
  33. Pedersen EB. Angiotensin-converting enzyme inhibitor renography. Pathophysiological, diagnostic and therapeutic aspects in renal artery stenosis. Nephrol Dial Transplant 1994; 9:482.
  34. Setaro JF, Saddler MC, Chen CC, et al. Simplified captopril renography in diagnosis and treatment of renal artery stenosis. Hypertension 1991; 18:289.
  35. Mann SJ, Pickering TG. Detection of renovascular hypertension. State of the art: 1992. Ann Intern Med 1992; 117:845.
  36. van Jaarsveld BC, Krijnen P, Derkx FH, et al. The place of renal scintigraphy in the diagnosis of renal artery stenosis. Fifteen years of clinical experience. Arch Intern Med 1997; 157:1226.
  37. Krijnen P, van Jaarsveld BC, Deinum J, et al. Which patients with hypertension and atherosclerotic renal artery stenosis benefit from immediate intervention? J Hum Hypertens 2004; 18:91.
  38. van Onna M, Houben AJ, Kroon AA, et al. Asymmetry of renal blood flow in patients with moderate to severe hypertension. Hypertension 2003; 41:108.
  39. Roubidoux MA, Dunnick NR, Klotman PE, et al. Renal vein renins: inability to predict response to revascularization in patients with hypertension. Radiology 1991; 178:819.
  40. Vaughan ED Jr. Curable renal hypertension: renin, marker or cause? Question answered. Am J Hypertens 2014; 27:1000.
  41. Strong CG, Hunt JC, Sheps SG, et al. Renal venous renin activity. Enhancement of sensitivity of lateralization by sodium depletion. Am J Cardiol 1971; 27:602.
  42. Rossi GP, Cesari M, Chiesura-Corona M, et al. Renal vein renin measurements accurately identify renovascular hypertension caused by total occlusion of the renal artery. J Hypertens 2002; 20:975.
  43. Pedersen EB. New tools in diagnosing renal artery stenosis. Kidney Int 2000; 57:2657.
  44. Hicks CW, Clark TWI, Cooper CJ, et al. Atherosclerotic Renovascular Disease: A KDIGO (Kidney Disease: Improving Global Outcomes) Controversies Conference. Am J Kidney Dis 2022; 79:289.
  45. Elkohen M, Beregi JP, Deklunder G, et al. A prospective study of helical computed tomography angiography versus angiography for the detection of renal artery stenoses in hypertensive patients. J Hypertens 1996; 14:525.
  46. Garovic VD, Textor SC. Renovascular hypertension and ischemic nephropathy. Circulation 2005; 112:1362.
  47. Scolari F, Ravani P. Atheroembolic renal disease. Lancet 2010; 375:1650.
  48. Chi YW, White CJ, Thornton S, Milani RV. Ultrasound velocity criteria for renal in-stent restenosis. J Vasc Surg 2009; 50:119.
  49. De Bruyne B, Manoharan G, Pijls NH, et al. Assessment of renal artery stenosis severity by pressure gradient measurements. J Am Coll Cardiol 2006; 48:1851.
  50. Leertouwer TC, Pattynama PM, van den Berg-Huysmans A. Incidental renal artery stenosis in peripheral vascular disease: a case for treatment? Kidney Int 2001; 59:1480.
  51. Choudhri AH, Cleland JG, Rowlands PC, et al. Unsuspected renal artery stenosis in peripheral vascular disease. BMJ 1990; 301:1197.
  52. Marcantoni C, Zanoli L, Rastelli S, et al. Effect of renal artery stenting on left ventricular mass: a randomized clinical trial. Am J Kidney Dis 2012; 60:39.
Topic 3825 Version 28.0

References

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