Gray, Bruce H
The treatment options for renal artery stenosis include bypass surgery, surgical endarterectomy, or balloon angioplasty with/without stenting. Each of these procedures is delivered today with differing frequency, morbidity/mortality, and outcomes. The procedure most applicable to patients with atherosclerotic disease is percutaneous transluminal renal angioplasty with stenting. Stents prevent plaque recoil, minimizing early restenosis, and the relatively large size of the renal artery (5–7 mm) minimizes late stent restenosis rates. The clinical features that help predict a favorable response to intervention are reviewed. In short, intervention provides a durable means to control renovascular hypertension, ischemic nephropathy, and congestive heart failure due to poor renal volume control.
The development of percutaneous transluminal renal artery angioplasty (PTRA) with or without stenting has substantially altered the treatment of renovascular disease. Before 1998, only approximately 10 revascularizations were performed each year by the Vascular Surgery Department at my institution, all of which were open surgical procedures [1]. This pattern changed significantly with the introduction of PTRA with renal artery stenting (PTRAS). In 1998, 22 revascularizations were performed, 10 surgical and 12 using PTRAS [1]. This increase in revascularizations continued in subsequent years. Within 4 years, the number of revascularizations had increased approximately sevenfold; 90% of these revascularizations were performed using PTRAS [1]. This increase occurred without any change in the indication for revascularization. Clinical diagnoses of hypertension, renal insufficiency, and pulmonary edema, as well as the number of blood pressure medications and serum creatinine levels before revascularization, were similar for surgical and endovascular procedures [1]. Morbidity and mortality, however, were decreased with endovascular repair. In this series, the range of surgical morbidity was 15–23.6%, and that for surgical mortality was 8.1–9.1% depending on whether the procedure involved an isolated renal revascularization or a combined aortorenal revascularization. In contrast, endovascular repair had a 5.6% morbidity and no mortality (both P < 0.05 compared with either surgical revascularization) [1]. Although these results will vary from one institution to the next depending on the skill of the surgical and interventional teams, it is clear that there is a difference in overall risk between open abdominal surgery and a femoral or brachial artery stick with catheter manipulation. As a result, the trend has shifted, with most institutions adopting PTRAS as the initial revascularization of choice.
This change is not surprising. In 1993, a randomized trial of PTRA versus surgery demonstrated that although technical success and primary patency were better with surgery, secondary patency rates and effects on blood pressure and renal function were similar [2]. PTRA was associated with a trend for a lower number of major complications (P = 0.17) [2]. The authors therefore recommended PTRA, combined with intensive follow-up and aggressive reintervention when indicated, as first-line therapy for renovascular disease [2].
Plaque recoil is the major complication associated with PTRA. Stent placement at the time of angioplasty should logically address this problem without significantly increasing morbidity or mortality. In 1999, van de Ven et al. [3] randomized 85 patients with > 50% renal artery stenosis to treatment with PTRA or PTRAS. Compared with PTRA, PTRAS significantly improved primary and secondary patency rates and reduced the restenosis rate without significantly increasing procedural complications [3]. Stenting, not balloon angioplasty, is probably the single most significant factor in the shift from surgical to percutaneous treatment of renovascular disease.
The kidney has three primary functions: it regulates blood pressure, controls volume, and filters out impurities. Revascularization is indicated when renal artery stenosis significantly compromises one or more of these three functions The probability that renovascular hypertension will respond to revascularization is increased in patients with: (1) hypertension presenting before age 30 or after age 60; (2) a recent onset or a recent change in preexisting hypertension; and (3) refractory, accelerated, or malignant hypertension. Similarly, the chance for renal salvage is increased in patients with: (1) unexplained renal failure or renal failure that is induced by angiotensin-converting enzyme inhibitors or angiotensin receptor blockers; (2) loss of renal mass over time documented by magnetic resonance imaging or duplex ultrasonography; and (3) established progression of renal artery stenosis. Revascularization in these patients typically permits the subsequent use of angiotensin-converting enzyme inhibitors, improving hypertension management. Finally, cardiac disturbance syndrome, a new label that has gained prominence, describes patients with problems in volume control, leading to recurrent congestive heart failure (CHF) and/or flash pulmonary edema. When these symptoms are caused by renal artery stenosis, revascularization significantly reduces symptoms.
When these symptoms are absent, medical, not interventional, therapy should be pursued. In general, medical therapy is indicated in patients who have mild hypertension, a satisfactory blood pressure response to drug therapy, and good renal function that remains stable over time . In addition, advanced age, the presence of significant comorbidities, and anatomic restrictions or other factors that increase the risk of revascularization all favor continued medical therapy over revascularization.
Revascularization is warranted only in patients with sufficient renal artery stenosis to produce significant hypertension, volume-related symptoms, or threat to renal viability. In 1962, Haimovici and Zinicola [4] evaluated the hemodynamic effects of graded extraluminal renal artery constriction in a dog model. There were no hemodynamic effects when vessel diameter was reduced <= 60% (84% reduction in cross-sectional area); however, reductions beyond this point (> 60%) produced a sudden and marked change in blood pressure distal to the constriction [4]. These findings were recently confirmed using a miniaturized pressure guide wire in patients with renal artery stenosis [5]. The development of the miniaturized pressure guide wires permits determination of gradients with great precision [5]. In this evaluation, there was a significant curvilinear correlation (r = 0.9, P < 0.01) between the systolic pressure gradient and the stenosis diameter [5]. The breakpoint in this relationship appeared at a stenosis severity of ~50% corresponding to a 22-mmHg pressure gradient, with a rapid acceleration in pressure gradient for stenoses beyond this level [6]. Intervention will probably have a beneficial effect on blood pressure and/or renal function only in patients with a hemodynamically significant stenosis, indicated by a >= 20-mmHg pressure gradient measured before intervention.
Finally, the type and location of the renal artery disease are significant when considering intervention. In addition to atherosclerosis, many disorders such as fibromuscular dysplasia (discussed later), vasculitis, spontaneous dissection, aneurysmal disease, William's syndrome, neurofibromatosis, and trauma can produce renal artery stenosis and significantly influence its treatment. Significant variations exist even among patients with atherosclerotic disease. Very brittle atherosclerosis in the elderly responds well to balloon dilation, whereas the caseous atherosclerosis in diabetic patients does not. The location of the stenosis determines the response to intervention. Approximately 75% of atherosclerotic disease is unilateral or bilateral ostial renal artery stenosis, 20% is nonostial stenosis, and 5% is segmental or isolated branch vessel disease.
Fibromuscular dysplasia occurs mostly in hypertensive patients who are female and/or < 30 years of age. This dysplasia can be intimal, medial, or perimedial. Intimal hyperplasia occurs in < 5% of patients with fibromuscular dysplasia, typically young children, is usually unilateral, and produces a stenosis that has a focal hourglass appearance. The most common form, medial fibroplasia, occurs in approximately 85% of patients with fibromuscular dysplasia; it is usually bilateral and produces a ‘string-of-beads’ appearance. The remaining 10% with fibromuscular dysplasia have perimedial fibroplasia, which is usually unilateral, produces the appearance of small beads, and typically does not enter into segmental arteries.
For the most part, endovascular treatment of fibromuscular dysplasia is quite successful with success rates of 75%, 92%, and 85%, and recurrence rates of 20%, 5%, and 10% for intimal, medial, and perimedial lesions, respectively [7]. Failure of endovascular therapy is typically related to the presence of aneurysms or very distal segmental disease. Surgical revascularization is also very effective with 80–90% success rates [8]. However, nephrectomy may be required in patients with irreparable ischemic atrophy or a hypoplastic ‘pressor’ kidney.
Although randomized controlled trials comparing endovascular repair with surgical repair have not been performed, they are probably not necessary in this disorder. Endovascular treatment is a low-risk procedure, and general anesthesia is not indicated; it is less invasive, requires a shorter hospital stay, has a success rate that is similar to that of surgical treatment, and does not preclude a subsequent surgical repair. Although the initial treatment of choice is endovascular repair, it is important to remember that these very fragile arteries must be handled carefully.
There are three basic types of surgical treatment for renovascular disease: nephrectomy, endarterectomy, or bypass (either anatomic or non-anatomic). Nephrectomy is straightforward. Recently, some surgeons have performed nephrectomy with a laparoscopic technique, further minimizing the risk. Endarterectomy involves direct removal of the atheroma. It is technically more demanding, carries a higher risk than other treatments, and is not performed at all centers. Anatomic bypass consists of inserting a tube graft from the aorta to one or both distal renal arteries. Although a common procedure in the past, it is now less common because surgical patients are older and have extensive aortic disease that requires simultaneous aortic replacement. Compared with isolated renal repair, it is associated with increased morbidity [1]. The extra-anatomic bypass is becoming more commonplace, especially in older patients. Performing a bypass graft from the hepatic artery to the right renal artery and/or transecting the splenic artery and transposing it to the left renal artery are “simpler” procedures that allow the surgeon to avoid manipulation of the diseased aorta.
The surgical management of renovascular disease has been significantly affected by the development of endovascular techniques. Most patients referred for surgery today are either unsuitable for or have already failed an attempted endovascular repair. These patients have more severe disease and/or more comorbidities than patients 10–15 years ago. In a recent review of 534 patients operated on at a single center over a 10-year period, 95% of the patients had diffuse extrarenal atherosclerotic disease, 80% had at least mild renal insufficiency, 60% had bilateral disease, and 40% required simultaneous aortic reconstruction [9]. The surgical approach to these patients must be based on the type and pattern of the renal artery disease as well as the clinical significance of the associated aortic lesions. In the recent review, 57% of the patients had an aortorenal bypass, 29% had endarterectomy, 7% had reimplantation, and 7% had nephrectomy [9].
As this review indicates, there is still a limited role for nephrectomy in the surgical management of renovascular disease. However, deciding when nephrectomy is indicated can be very difficult. In an evaluation of patients with renal artery occlusion, nephrectomy and revascularization were equally effective in managing hypertension, but only revascularization improved renal function significantly [10]. Furthermore, nephrectomy threatens global renal function if contralateral disease develops or progresses [10]. A management strategy that emphasizes revascularization over nephrectomy appears to provide the best opportunity for dialysis-free survival [10]. Nephrectomy should be limited to kidneys with negligible renal function (< 10% total renal function) and renal arteries that cannot be reconstructed [10]. Determining which kidneys meet this requirement may require multiple tests such as renal vein renin sampling, nuclear perfusion scan, and arteriographic imaging. In the preceding evaluation, 48% of patients were revascularized successfully, even in the absence of a nephrogram and/or distal reconstitution of their renal artery preoperatively [10].
Surgical treatment is generally effective, regardless of the type of procedure required [9]. In the previously discussed review, surgical mortality was 3.6%; 89% of the survivors had a beneficial blood pressure response (18% cured, 71% improved), and 50% had improved renal function, including 30 (81%) of 37 patients who were removed from dialysis dependence [9]. This improvement in renal function has been associated with improved survival [9]. The 11% of patients who suffered worsening of their renal function following surgery, however, remain a concern. A key issue in the surgical management of this disorder is the ability to determine which patients are likely to benefit from and which are likely to worsen from renal revascularization, as the risks are not inconsequential.
Finally, graft failure is a major complication. Even when performed surgically, not all revascularization procedures are successful. In a review of 323 renal artery revascularizations performed over a 15-year period, approximately 5% of the grafts failed within the first 30 days [11]. Overall, there were no significant differences in failure rates between anatomic and non-anatomic grafts; however, aortorenal bypass from the native aorta had a significantly higher failure rate (17.6%) than aortorenal bypass from an aortic graft (2%) [11]. Combining aortorenal bypass with aortic reconstruction significantly increased the prevalence of major complications (21.4%), leading the authors to recommend this procedure only when sufficient aortic disease already exists to merit replacement [11].
The Dutch Renal Artery Stenosis Intervention Cooperative (DRASTIC) trial is discussed in detail in Covit's article in this supplement, and will only be briefly reviewed here. This trial randomized patients with >= 50% renal artery stenosis and diastolic hypertension (despite treatment with two antihypertensive medications) to either medical therapy or balloon angioplasty without stent placement. Patients were followed for 1 year, and the data were subsequently analyzed on an intent-to-treat basis [12]. By 3 months, 44% of the medical group had failed this therapy and crossed over to PTRA [12]. This high crossover rate significantly impacts the assessment of the effects of medical versus interventional therapy in this trial. In addition, excluding stenting as an option in the study design reduced the potential efficacy of interventional therapy.
As previously discussed, van de Ven et al. [3] demonstrated that PTRAS significantly improves primary and secondary patency rates and reduces restenosis rates compared with PTRA alone. Consistent with these findings, restenosis of the renal artery developed in 48% of the patients randomized to interventional therapy in the DRASTIC study [12], potentially limiting the efficacy of this therapy. Despite this, hypertension was cured in 7% of the patients randomized to PTRA compared with none of the patients randomized to medical therapy [12]. Overall, however, both treatments in this study must be considered failures since neither controlled blood pressure to current Joint National Committee on Prevention, Detection, Evaluation, and Treatment of High Blood Pressure standards [13] or European standards [14]. After 12 months of therapy, mean blood pressures were 163/96 and 160/93 mmHg in the medical and surgical groups, respectively [12]. We need to understand how to treat these patients more effectively.
This lack of understanding is also demonstrated by some of the results in the van de Ven et al. trial [3]. Despite significant differences in patency and restenosis rates, no significant differences were detected in either blood pressure or renal function response [3]. There was a trend for greater improvement in these parameters with PTRAS, and this failure to detect a significant difference may simply reflect that this study was inadequately powered to evaluate these other parameters [3]. Nonetheless, it is still surprising that significant differences were not detected given the 48% restenosis rate for PTRA compared with the 14% for PTRAS [3]. While we do not have all the answers on how the kidneys are affected, I still believe that primary stenting is better than secondary stenting for ostial renal artery disease. To achieve results similar to those with primary PTRAS, a strategy of PTRA followed by secondary stenting, when necessary, would require 45% more hospital admissions for reintervention procedures, thus increasing the risk of complications [3].
Most of the complications of endovascular repair are minor and occur at the vascular access site (femoral artery and, more commonly, brachial artery). Although catastrophic events requiring urgent surgical repair or nephrectomy can occur, these events are rare. If they occur, most perforations or dissections can be treated with an additional stent or a covered stent graft without surgery. Preventing atheroemboli, however, can be challenging. Although these emboli may be ubiquitous to all patients with atherosclerotic renal artery disease and may be occurring prior to intervention, catheter manipulation can escalate this problem, leading to deterioration in renal function. However, there are techniques that can be used during the diagnostic evaluation and interventional procedure to minimize this risk. All catheter manipulation, including reshaping of the catheter, should be carried out below the level of the renal arteries, with the catheter then gradually walked up to the renal artery. This avoids, or at least minimizes, the chance of aortic plaque shedding into the renal arteries. The probability of a significant chunk of atherosclerotic plaque embolizing into the renal artery is low. Current embolic protection devices have limited efficacy since they can only be protective during part of the procedure. They cannot prevent emboli from reaching the kidney during initial catheter manipulation, during arteriography, or from the aorta after the procedure. Without further refinements, the role of embolic protection devices will be limited.
Endovascular treatment of renal artery stenosis can significantly improve blood pressure control, volume status, and renal function in appropriate patients. The key issue is being able to prospectively identify these patients. Several factors that could potentially influence treatment success or failure have been evaluated. One such factor is the resistance to flow in segmental renal arteries, quantified as the renal resistance index. In one evaluation of 35 patients, a renal resistance index >= 80% or 0.8 was associated with a lack of improvement in blood pressure and a worsening of renal function following revascularization [15]. However, data from more recently treated patients contradict these findings [16].
Zeller et al. [16] evaluated 241 consecutive patients with severe (>= 70%) ostial renal artery stenosis treated with PTRAS; 41% of the study population had diabetes mellitus and 73% had nephrosclerosis, defined as a renal resistance index >= 80% or 0.8. All treatments were technically successful, and there was no procedure-related mortality [16]. Subsequent results were evaluated using 24-h ambulatory blood pressure monitoring and serum creatinine levels [16]. Overall, the mean follow-up period was 27 months, during which time 10% of the patients with treated arteries developed restenosis and 9% of the patients died [16]. In this study, PTRAS produced significant improvements in both renal function and blood pressure in patients with mild to moderate (renal resistance index: 0.7-0.8) and severe (renal resistance index: > 0.8) nephrosclerosis and produced significant improvements in blood pressure in patients without nephrosclerosis [16]. This study demonstrates that intervention can significantly improve blood pressure and renal function, and calls into question the predictive power of the renal resistive index.
The more severe the baseline abnormality, the greater the improvements tend to be. In an evaluation of 215 consecutive patients with severe ostial renal artery stenosis, mean arterial blood pressure (P < 0.001), parenchymal/pelvic ratio >= 1 (P = 0.036) (an ultrasonographic marker of normal parenchymal thickness), and female gender (P = 0.032) were independent predictors of blood pressure improvement; serum creatinine (P = 0.004) and left ventricular function (P = 0.032) were independent predictors of renal function improvement following PTRAS [17]. A significant improvement in serum creatinine levels occurred only in patients with baseline levels > 1.5 mg/dl (P = 0.025) [17]. This improvement in renal function has a significant effect on mortality. As discussed in this supplement, renal dysfunction increases mortality, and interventions that reduce this dysfunction significantly improve survival [18].
Patients with the cardiac disturbance syndrome are also likely to benefit from interventional therapy. In 39 patients with recurrent episodes of CHF and flash pulmonary edema who had severe (> 70%) bilateral renal artery stenosis or severe stenosis to a solitary kidney, PTRAS significantly decreased the number of hospital admissions for CHF (P < 0.001; Fig. 5). In fact, 30 of these 39 patients (77%) had no subsequent admissions during a mean 21-month follow-up [19]. The mean New York Heart Association functional class decreased from 2.9 at baseline to 1.6 following PTRAS (P < 0.001); 28 patients (72%) had improved blood pressure control, and 20 patients (51%) had improved serum creatinine levels [19]. Of note, 10 patients had a serum creatinine level >= 4.0 before PTRAS, and renal function improved in six of these patients [19].
Although endovascular therapy is generally the appropriate first intervention, special circumstances can make surgery the preferred treatment in selected patients. If the patient needs abdominal surgery to repair an aneurysm, revascularization of the renal artery should probably be performed at the same time, if it can be performed safely. The question of whether to add the additional risk of PTRA or PTRAS to the surgery is a decision that centers on the balance between the perceived increase in surgical risk from prolonging the operative procedure versus the perceived risk of a percutaneous procedure. These risks, like cardiac risk, differ for each patient and must be carefully weighed in a patient-specific manner.
The size of the renal arteries is also a special consideration. My experience is that the restenosis rate is approximately 40% for renal arteries <= 4 mm, is 14-18% for renal arteries of 5.0-5.5 mm, and is < 10% for renal arteries >= 6 mm. This restenosis rate is similar to a previously published rate, except that the rate for arteries <= 4 mm was only 16% in that study [20]. Given the high restenosis rate for renal arteries <= 4 mm and knowing that surgical revascularization is highly effective in these arteries, a primary surgical approach is probably preferable in these patients.
Patients with severe ulcerative and friable atheroma have very fragile vessels that may show contrast staining simply from a diagnostic contrast injection near the renal artery. These vessels should not be entered with a catheter, and surgery is clearly preferable in these patients.
An endovascular approach works best for discrete isolated stenoses. Surgery is probably preferable in patients with long, diffuse renal artery lesions or in branch (segmental) intrarenal disease. Similarly, surgery is probably preferable in patients with renal artery occlusion since endovascular therapy is more complex with greater risk. Finally, it may be preferable to surgically bypass the diseased area in some patients with recurrent stenosis following angioplasty or stenting, although most of these patients can be retreated with angioplasty or stenting.
The overall treatment algorithm for renal artery stenosis is relatively simple (Fig. 6). First, determine whether the patient has an indication for revascularization. If there are no indications for revascularization, then treat medically and reassess continually. If there are indications for revascularization, determine whether the patient has any special consideration that would make surgery preferable to endovascular treatment. If yes, refer the patient for surgery; otherwise, proceed with PTRAS. Finally, after either surgery or PTRAS, all patients require optimal medical treatment and continued reassessment. These evaluations and reassessments should be performed every 3–6 months for the first year and at least yearly thereafter.
Patients must have significant symptoms
(hypertension, CHF, pulmonary edema, azotemia, or shrinkage of the kidney)
attributable to renal artery stenosis before intervention therapy is considered.
The hemodynamic significance of the stenosis must be established by determining
the pressure gradient across the stenotic region. Typically, pressure gradients
>= 20 mmHg are necessary before a lesion becomes hemodynamically significant.
The whole patient must be considered when selecting the appropriate
interventional therapy. For most of these patients, PTRAS will be the treatment
of choice.
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