Version May 2024
INTRODUCTION — Renal artery stenosis is a relatively common finding in older patients with hypertension. However, renal artery stenosis is the primary cause of hypertension (ie, renovascular hypertension) only in certain settings.
In most cases of renal artery stenosis, one kidney is affected with the second kidney being essentially normal, hence the designation "unilateral" disease. Individuals with high-grade stenosis to both kidneys, or to a solitary functioning kidney thereby affecting the entire functioning kidney mass, are considered to have "bilateral" disease. Bilateral renal artery stenosis, or stenosis to a solitary functioning kidney, merits specific consideration because of its additional contribution to fluid retention, loss of kidney function, and heart failure.
The treatment of bilateral atherosclerotic renal artery stenosis (or stenosis of a solitary functioning kidney) will be reviewed here. Clinical clues suggesting the presence of renovascular hypertension and establishing the diagnosis of renal artery stenosis, treatment of unilateral atherosclerotic renal artery stenosis, issues related to chronic kidney disease associated with atherosclerotic renovascular disease, and diagnosis and treatment of fibromuscular disease are presented in detail elsewhere:
●(See "Evaluation of secondary hypertension".)
●(See "Establishing the diagnosis of renovascular hypertension".)
●(See "Treatment of unilateral atherosclerotic renal artery stenosis".)
●(See "Chronic kidney disease resulting from atherosclerotic renal artery stenosis".)
●(See "Clinical manifestations and diagnosis of fibromuscular dysplasia".)
●(See "Treatment of fibromuscular dysplasia of the renal arteries".)
REVIEW OF PRESENTATION AND DIAGNOSIS
Epidemiology — The prevalence of renovascular hypertension is probably less than 1 percent in patients with mild hypertension but may be as high as 10 to 40 percent in patients with acute hypertension (even if superimposed on a preexisting elevation in blood pressure), severe hypertension (eg, blood pressure >180 mmHg systolic and/or >110 mmHg diastolic), or refractory hypertension [1]. (See "Evaluation of secondary hypertension", section on 'Clinical clues for renovascular hypertension'.)
In prospective treatment trials of patients with renal artery stenosis, the prevalence of bilateral disease (rather than unilateral disease) ranged from 23 to 54 percent [2-4]. Rarely are both arteries affected with stenosis to an identical degree. Some patients with unilateral disease managed primarily with medical therapy present at a later stage with bilateral atherosclerotic disease due to disease progression.
Bilateral renal arterial stenosis is associated with more widespread atherosclerotic disease, higher serum creatinine levels, and higher mortality than unilateral disease [5,6]. (See "Chronic kidney disease resulting from atherosclerotic renal artery stenosis".)
Etiology — There are two major causes of bilateral renal artery stenosis:
●Atherosclerosis – Atherosclerosis primarily affects patients over the age of 45 years and usually involves the aortic orifice or the proximal main renal artery. This disorder is particularly common in patients with diffuse atherosclerosis [7] but can occur as an isolated kidney lesion. (See "Chronic kidney disease resulting from atherosclerotic renal artery stenosis".)
●Fibromuscular dysplasia – In contrast to atherosclerosis, fibromuscular dysplasia (FMD) most often is identified in females under the age of 50 years and typically involves the mid- or distal main renal artery or the intrarenal branches [8]. (See "Clinical manifestations and diagnosis of fibromuscular dysplasia" and "Treatment of fibromuscular dysplasia of the renal arteries".)
Since the advent of endovascular aortic stent grafts, renal artery stenosis may also result from migration and/or placement of these stents over the renal orifices. Less common etiologies include renal artery dissection or inflow stenosis to a kidney allograft. (See "Endovascular repair of abdominal aortic aneurysm".)
Clinical clues — There are a number of clinical findings that suggest an increased likelihood of secondary hypertension, some of which specifically suggest the presence of renovascular disease. These findings are used clinically to determine which patients should be evaluated for renovascular disease (table 1). In addition, bilateral atherosclerotic renal artery stenosis or unilateral disease in a single viable kidney can be associated with progressive kidney dysfunction (called chronic ischemic renovascular disease or "ischemic nephropathy") [9]. (See "Chronic kidney disease resulting from atherosclerotic renal artery stenosis".)
Some of these clinical clues are relatively specific for the presence of renovascular disease, and some help to identify those patients who are more likely to benefit from intervention. As examples:
●A recent or rapid progression of severe hypertension. This finding is relatively specific for renovascular hypertension and is the strongest predictor of antihypertensive benefit from revascularization.
●A rapid rise in arterial pressure associated with sudden development of left ventricular failure (occasionally referred to as "flash pulmonary edema") [10,11]. This finding is more common with bilateral as compared with unilateral renal artery stenosis because bilateral disease is also associated with diuretic resistance and sympathetic adrenergic activation [11].
●Rapidly changing serum creatinine levels, particularly following administration of angiotensin-converting enzyme (ACE) inhibitors or angiotensin II receptor blockers (ARBs). The rise in serum creatinine is more common with agents that block the renin-angiotensin system than with other antihypertensive drugs because glomerular filtration rate (GFR) often depends upon the efferent arteriolar actions of angiotensin II in this setting. This finding is also more common with bilateral as compared with unilateral disease because there is hemodynamic compromise to the entire kidney functional mass [12]. Restoring the renal blood supply in such cases can restore the ability to use these drugs for blood pressure control.
These clinical clues, as well as the indications for testing to establish the diagnosis of renal artery stenosis, are presented in detail in other topics. (See "Evaluation of secondary hypertension" and "Establishing the diagnosis of renovascular hypertension", section on 'Indications for testing'.)
Advances in contrast imaging (computed tomography [CT] and magnetic resonance [MR] angiography) and Doppler ultrasound have led to the identification of renal arterial stenosis as an "incidental finding" more commonly than before [13]. Although some may develop progressive disease, the absence of clinical clues for renovascular hypertension in such patients substantially reduces the likelihood that the renal artery stenosis is responsible for hypertension, if present, and also reduces the likelihood of benefit from percutaneous or surgical intervention [14-17]. (See 'Medical therapy' below and "Establishing the diagnosis of renovascular hypertension", section on 'Incidental lesions'.)
Diagnosis — The diagnosis of renal artery stenosis is made by imaging studies in patients thought to be at risk. 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 more important threshold. With CT and MR angiography, a stenosis greater than 75 percent in both renal arteries, or 50 percent stenosis with poststenotic dilatation, suggests that the patient may have clinically significant bilateral renal artery stenosis. These issues are discussed in detail separately. (See "Establishing the diagnosis of renovascular hypertension".)
RISK FACTOR REDUCTION — Patients with atherosclerotic renovascular disease have a high prevalence of systemic atherosclerosis and are at increased risk for adverse cardiovascular outcomes. As a result, they are considered to have a coronary artery disease equivalent and should be treated accordingly for secondary prevention of cardiovascular disease (eg, statin and aspirin therapy, blood pressure control, smoking cessation). (See "Prevention of cardiovascular disease events in those with established disease (secondary prevention) or at very high risk".)
TREATMENT
General approach to therapy — Once a diagnosis of bilateral hemodynamically significant renal artery stenosis (or hemodynamically significant stenosis in a solitary functioning kidney) is established, there are three therapeutic alternatives:
●Medical therapy alone
●Percutaneous renal angioplasty, usually with stent placement, in addition to medical therapy
●Surgical revascularization in addition to medical therapy
Medical therapy for control of hypertension is indicated in all patients with bilateral renal artery stenosis (or unilateral stenosis in a single viable kidney) [15-18]. Revascularization, usually by percutaneous angioplasty with stenting, is reasonable in patients who have a high likelihood of benefitting from intervention [15,16]. The following scenarios identify such patients:
●A short duration 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
●Intolerance to optimal medical therapy (eg, deterioration of kidney function during antihypertensive drug therapy)
●Recurrent flash pulmonary edema and/or refractory heart failure
●Otherwise unexplained progressive kidney function impairment, particularly if proteinuria is absent
The data supporting this approach are presented elsewhere in detail:
●(See "Chronic kidney disease resulting from atherosclerotic renal artery stenosis".)
In patients selected for revascularization, endovascular stent placement is most commonly employed if technically feasible. Surgery is primarily warranted for correction of complex vascular lesions and/or repeated episodes of in-stent restenosis.
Revascularization versus medical therapy alone — The randomized trials and meta-analyses that compared revascularization using angioplasty (with or without stent) plus medical therapy versus medical therapy alone are presented elsewhere in detail. (See "Treatment of unilateral atherosclerotic renal artery stenosis", section on 'Revascularization versus medical therapy alone'.)
Patients with bilateral renal artery stenosis were included in most of these trials (ranging from 23 to 54 percent of enrolled patients). Only one study excluded patients with bilateral disease. In general, the effects of revascularization on blood pressure were greater in bilateral disease, but effects on kidney function and mortality did not differ in those with bilateral as compared with unilateral stenosis [19].
The limitations of these data are also presented elsewhere but are briefly repeated here [20] (see "Treatment of unilateral atherosclerotic renal artery stenosis", section on 'Revascularization versus medical therapy alone'):
●The number of patients with hemodynamically significant bilateral renal artery stenosis (more than 75 percent of both arteries) was limited since many lesions were characterized by 50 to 70 percent stenosis. In addition, in one trial, many patients were incorrectly identified as having renal artery stenosis greater than 50 percent [3]. Similarly, data from the Cardiovascular Outcomes of Renal Atherosclerotic Lesions (CORAL) trial confirmed that clinicians frequently overestimate the degree of stenosis substantially, even when quantitative estimates are performed [4].
●Patients in these trials were not selected because they had clinical clues (mentioned above) suggesting that the stenosis was likely to contribute to the hypertension or chronic kidney disease (table 1). This is a potentially important issue since bilateral (or unilateral) atherosclerotic renovascular disease can be an incidental finding on angiography for peripheral artery disease [13,21].
●The early trials directed at renovascular hypertension had crossover rates from the medical therapy alone group to the revascularization group ranging from 20 to 44 percent due to failure of blood pressure control with medical therapy alone.
Overview of therapeutic options — The following discussion will review the antihypertensive response to therapy in patients with bilateral renal artery stenosis. The effects of revascularization on preservation of kidney function in such patients are discussed separately. (See "Chronic kidney disease resulting from atherosclerotic renal artery stenosis".)
Medical therapy — Bilateral renal hypoperfusion induces activation of the renin-angiotensin-aldosterone system and impairs sodium excretion resulting in expansion of the extracellular fluid volume. Both of these factors contribute to the ensuing rise in blood pressure. As a result, combination therapy with a diuretic plus an angiotensin-converting enzyme (ACE) inhibitor or angiotensin II receptor blocker (ARB) can control the hypertension in most patients with bilateral renal artery stenosis and is likely to be more effective than other antihypertensive therapy. In a Canadian cohort study, for example, patients with renal artery stenosis who were prescribed ACE inhibitors were significantly less likely to die or have a myocardial infarction or stroke (10 versus 13 events per 100 patient-years) as compared with similar patients prescribed other therapy [22]. ACE inhibitor therapy was also associated with a lower risk of end-stage kidney disease but a higher risk of acute kidney injury (1.2 versus 0.6 events per 100 patient-years).
Acute kidney injury, which is hemodynamically mediated, is the major limitation of ACE inhibitors and ARBs in patients with bilateral renal artery stenosis. Because of the stenotic lesion, lowering the systemic blood pressure is more likely to reduce the kidney perfusion and intraglomerular pressure below the limits of autoregulation; this will tend to lower the glomerular filtration rate (GFR) (figure 1). The usual autoregulatory response in this setting includes an increase in efferent (postcapillary) arteriolar resistance, which is mediated in part by angiotensin II [23]. Blocking the action of angiotensin II with an ACE inhibitor or ARB blunts this autoregulatory response and tends to reduce the GFR (figure 2) [23]. This effect is more pronounced in patients with diuretic-induced volume depletion since the hypovolemia induces an increase in angiotensin II; the GFR in such settings is more angiotensin II dependent than in patients without hypovolemia [24]. (See "Renal effects of ACE inhibitors in hypertension".)
The net effect is that therapy with an ACE inhibitor or ARB in some patients with significant bilateral renal artery stenosis can produce a rise in the serum creatinine concentration [24]; this may also occur in some patients with less severe bilateral disease. However, these observations do not mean that ACE inhibitors and ARBs are contraindicated in this disorder as long as the patient is carefully monitored. The decline in GFR is small in most patients; a large increase in the serum creatinine concentration (by more than 30 percent above the previous baseline value) occurs in less than 5 to 10 percent of cases, and the majority of patients (78 percent in one series) with severe bilateral stenosis can tolerate an ACE inhibitor or ARB [25]. In addition, kidney function can be improved in many patients by discontinuing the diuretic [26] and, in most cases, by discontinuing the ACE inhibitor or ARB [20]. (See "Renal effects of ACE inhibitors in hypertension".)
Although a rise in serum creatinine induced by antihypertensive therapy is more common with ACE inhibitors and ARBs, some patients with severe bilateral disease have developed acute kidney injury after the initiation of any antihypertensive agent (figure 3) [27]. Such patients have reached a critical limit of kidney perfusion, and both systemic blood pressure control and stable kidney function cannot be simultaneously achieved. Restoring renal blood flow with either endovascular or surgical techniques in these cases is required to protect kidney function and control the blood pressure.
There are two primary concerns in patients treated with medical therapy alone:
●Chronic normalization of the systemic pressure that might eventually lead to ischemic atrophy due to the reduced kidney perfusion pressure distal to the stenosis. The risk of this complication and whether it is more likely to occur with an ACE inhibitor are unresolved. In two randomized trials of patients with renal artery stenosis, renal events (usually defined as doubling of the serum creatinine and/or progression to advanced chronic kidney disease) developed in 16 to 22 percent of subjects followed between two and four years [2,3]. (See "Treatment of unilateral atherosclerotic renal artery stenosis", section on 'Loss of functional kidney mass in the stenotic kidney'.)
●Progression of stenosis in those with atherosclerotic disease. Studies in which repeat duplex ultrasonography or serial angiograms were performed have reported rates of progressive stenosis ranging from 11 to 44 percent at two to four years. However, the incidence of progression may be as high as 60 percent in patients with bilateral stenosis or stenosis of a solitary functioning kidney. The data are presented elsewhere in detail. (See "Treatment of unilateral atherosclerotic renal artery stenosis", section on 'Progression of stenosis'.)
Additional issues of progression of renal artery stenosis and medical therapy risks in patients with bilateral renal artery stenosis are discussed in detail separately. (See "Chronic kidney disease resulting from atherosclerotic renal artery stenosis".)
Percutaneous transluminal renal angioplasty and stenting — Initial observational studies showed a high rate of procedural success with percutaneous transluminal renal angioplasty (PTRA) and stent placement in patients with ostial atherosclerotic disease, as well as a high rate of clinical success measured by improvements in blood pressure and kidney function in 50 to 75 percent of subjects [28-32]. Individual case reports and small series confirmed that PTRA with stenting could sometimes improve kidney function, resolve hypertension, and diminish episodes of heart failure [33,34]. (See "Chronic kidney disease resulting from atherosclerotic renal artery stenosis".)
As noted above, however, randomized trials showed no additional benefit from PTRA when added to medical therapy with respect to blood pressure control, kidney function, cardiovascular events, and mortality. The results from these trials and their limitations are briefly presented above and discussed elsewhere in detail. (See 'Revascularization versus medical therapy alone' above and "Treatment of unilateral atherosclerotic renal artery stenosis", section on 'Revascularization versus medical therapy alone'.)
Some of these limitations were addressed in the CORAL trial; specifically, enrolled patients were initially required to have at least 80 percent stenosis of one or more renal arteries, or 60 percent stenosis combined with documentation of a pressure drop across the stenosis [31]. However, recruitment into this and other trials for renal artery stenosis was problematic and resulted in adjustment of the entry criteria during the study, partly as a result of the experience from previous trials and reluctance to enroll patients with more severe disease [35]. The average stenosis reported from the angiographic core laboratory in CORAL was 67 percent; fewer than 20 percent of patients had a stenosis greater than 80 percent [4].
Stent placement — In patients undergoing PTRA for treatment of atherosclerotic renal artery stenosis, we suggest stent placement when feasible. Stent placement produced superior technical success in a trial of 85 patients (42 with bilateral disease) assigned to PTRA alone or PTRA combined with stent. The data are presented elsewhere. (See "Treatment of unilateral atherosclerotic renal artery stenosis", section on 'Stent placement'.)
In addition, PTRA alone (ie, without stenting) is generally less successful and associated with more complications (such as atheroemboli) in patients with bilateral as compared with unilateral atherosclerotic renal artery stenosis, due in part to the frequent presence of ostial or completely occluding lesions, both of which are less amenable to routine PTRA [36].
Procedural complications — The technical complication rate with percutaneous transluminal renal angioplasty with or without stenting is between 5 and 15 percent [2,3,20,30,37-39]. Most of the complications are relatively minor and include puncture site hematoma and renal artery dissection. However, more serious problems can arise, including renal artery thrombosis or perforation (sometimes requiring surgery) and acute kidney injury due to atheroembolic disease (which may be irreversible) or to a reaction to the radiocontrast agent (which is usually reversible). Rarely, these complications lead to death.
In the ASTRAL trial described above, there were 38 complications that occurred within 24 hours of procedure in 31 of the 359 patients (9 percent) who underwent revascularization with stenting [2]. Nineteen of these events were serious, including pulmonary edema and myocardial infarction; there were five renal embolizations, four renal arterial occlusions, four renal artery perforations, one femoral-artery aneurysm, and three patients with clinically significant cholesterol embolization. Among 280 patients who underwent revascularization and for whom data were available, 20 percent had an adverse event between 24 hours and one month. These included two deaths, four cases of groin hematoma or hemorrhage, five cases of acute kidney injury, and one renal artery occlusion.
The overall incidence of clinically apparent atheroembolic disease following renal artery angioplasty is thought to be relatively low (1.2 percent in one large trial) but is probably higher in patients with bilateral disease and those with extensive aortic atherosclerosis [4,40]. However, the rate of atheroembolism associated with PTRA, particularly clinically silent atheroembolism, may be higher than previously thought. Studies of PTRA with stenting that have employed distal embolic protection devices have reported the capture of grossly visible material in 45 to 60 percent of cases [41,42]. Distal embolization of atheromatous material or thrombus could partially negate the benefits of revascularization on kidney function [43]. Whether performing the procedure with distal embolic protection results in improved kidney function is uncertain, as available reports are uncontrolled [3,44].
Surgery — Surgical revascularization (or removal of a completely occluded atrophic kidney) appears to have similar efficacy to percutaneous transluminal renal angioplasty in controlling blood pressure [45,46]. A number of different operative procedures can be used, including renal artery bypass from the aorta or a limited procedure (such as hepatorenal or splenorenal bypass) that avoids a diseased aorta. Most operations involve either bilateral repair or unilateral repair with contralateral nephrectomy of a nonfunctioning, atrophic kidney [46].
We agree with the 2005 American College of Cardiology/American Heart Association (ACC/AHA) guidelines and the 2022 American Heart Association Scientific Statement that surgery in patients with atherosclerotic renal artery stenosis and indications for revascularization be largely limited to those who have multiple small renal arteries, have early primary branching of the main renal artery, require aortic reconstruction near the renal arteries for other indications (eg, aneurysm repair or severe aortoiliac occlusive disease), or have failed renal artery stenting procedures or repeated in-stent restenosis [15,17,47].
In-hospital mortality associated with surgery — The potential benefits of surgery in these settings must be weighed against the operative mortality rate. In-hospital mortality following renovascular surgery in most reports has been between 3 and 7 percent, with the risk being increased in patients with diffuse atherosclerosis and heart failure [1,20,46]. However, most of these studies came from high-volume referral centers, which presumably have better outcomes with these procedures than low-volume centers.
A higher in-hospital mortality rate of 10.1 percent for atherosclerotic disease was noted in an analysis of over 6600 renal artery bypass graft procedures performed for hypertension or ischemic nephropathy from 2000 to 2004 in the United States; almost 70 percent were performed in teaching hospitals [48]. Independent risk factors for in-hospital mortality (relative risk 1.6 to 2.2) were advanced age and a history of chronic kidney disease, heart failure, or chronic lung disease. The mortality rate was similar with renal bypass graft alone or combined with abdominal aortic aneurysm repair or aortobifemoral bypass. There were no deaths in 105 procedures for fibromuscular dysplasia (FMD). (See "Treatment of fibromuscular dysplasia of the renal arteries", section on 'Surgery'.)
These observations provide support for percutaneous transluminal renal angioplasty with stenting as the preferred initial approach in most patients with bilateral atherosclerotic renal artery stenosis who are selected for revascularization [20,48] since hypertension and kidney outcomes appear to be similar to those attained with surgery [45]. In some cases, endovascular aortic repair can be undertaken with simultaneous fenestrated stent grafts to protect the renal circulation. Other patients who require aortic reconstruction near the renal arteries for other indications (eg, aneurysm repair or severe aortoiliac occlusive disease) may benefit from surgical renal revascularization [17]. Symptomatic coronary or cerebrovascular disease may need to be repaired prior to renovascular surgery, a strategy that can reduce overall mortality.
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 topic (see "Patient education: Renovascular hypertension (The Basics)")
SUMMARY AND RECOMMENDATIONS
●Overview – In most cases of renal artery stenosis, one kidney is affected with the second kidney being essentially normal, hence the designation "unilateral" disease. Individuals with high-grade stenosis to both kidneys, or to a solitary functioning kidney thereby affecting the entire functioning kidney mass, are considered to have "bilateral" disease. Bilateral renal artery stenosis, or stenosis to a solitary functioning kidney, merits specific consideration because of its additional contribution to fluid retention, loss of kidney function, and heart failure. (See 'Introduction' above.)
●Etiology – There are two major causes of bilateral renal artery stenosis (see 'Etiology' above):
•Atherosclerosis, which primarily affects patients over the age of 45 years and usually involves the aortic orifice or the proximal main renal artery. This disorder is particularly common in patients with diffuse atherosclerosis.
•Fibromuscular dysplasia (FMD), which most often affects females under the age of 50 years and typically involves the distal main renal artery or the intrarenal branches. (See "Clinical manifestations and diagnosis of fibromuscular dysplasia" and "Treatment of fibromuscular dysplasia of the renal arteries".)
●Manifestations – There are a number of clinical findings that suggest an increased likelihood of secondary hypertension, some of which specifically suggest the presence of renovascular disease (table 1). In addition, bilateral atherosclerotic renal artery stenosis or unilateral disease in a single viable kidney can be associated with progressive kidney dysfunction (called chronic ischemic renovascular disease or "ischemic nephropathy"). These clinical clues, as well as the indications for testing to establish the diagnosis of renal artery stenosis, are presented in detail in other topics. (See 'Clinical clues' above and "Evaluation of secondary hypertension" and "Chronic kidney disease resulting from atherosclerotic renal artery stenosis" and "Establishing the diagnosis of renovascular hypertension", section on 'Indications for testing'.)
Patients with atherosclerotic renovascular disease have a high prevalence of systemic atherosclerosis and are at increased risk for adverse cardiovascular outcomes. As a result, they are considered to have a coronary artery disease equivalent and should be treated accordingly for secondary prevention of cardiovascular disease. (See "Prevention of cardiovascular disease events in those with established disease (secondary prevention) or at very high risk".)
●Medical therapy – Antihypertensive therapy to control hypertension is indicated in all patients with bilateral renal artery stenosis (or unilateral stenosis in a single viable kidney). The data and specific recommendations are presented elsewhere. (See "Goal blood pressure in adults with hypertension".)
Angiotensin-converting enzyme (ACE) inhibitors and angiotensin II receptor blockers (ARBs) are effective in patients with bilateral renal artery stenosis; additional medications, such as diuretics, are frequently required. Potential concerns with the use of medical therapy without revascularization include acute kidney injury, long-term ischemic damage of the stenotic kidney, and progression of the stenosis. (See 'Medical therapy' above.)
●Interventional therapy – For patients with bilateral renal artery stenosis (or unilateral stenosis of a solitary functioning kidney) who meet one or more of the following five criteria, we suggest revascularization plus medical therapy rather than medical therapy alone (Grade 2C); revascularization is usually achieved by percutaneous angioplasty with stenting (or surgical revascularization in patients with complex anatomic lesions) (see 'General approach to therapy' above and 'Revascularization versus medical therapy alone' above):
•A short duration 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
•Intolerance to optimal medical therapy (eg, deterioration of kidney function during antihypertensive drug therapy)
•Recurrent flash pulmonary edema and/or refractory heart failure
•Otherwise unexplained progressive kidney function impairment
For patients with bilateral renal artery stenosis (or unilateral stenosis of a solitary functioning kidney) who do not meet one of the five criteria just listed, we suggest not revascularizing and instead treating with medical therapy alone (Grade 2B). (See 'General approach to therapy' above and 'Revascularization versus medical therapy alone' above.)
In patients undergoing percutaneous transluminal renal angioplasty (PTRA) for treatment of atherosclerotic renal artery stenosis, we suggest stent placement unless the anatomy precludes stenting (Grade 2B). (See 'Stent placement' above.)
Among patients who have an indication for renal artery revascularization, surgery is only preferred for selected patients who have complex anatomic lesions or have failed renal artery stenting procedures or repeated in-stent restenosis. (See 'Surgery' above.)
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