Adapted from: Haller C and Keim M. Current issues in the diagnosis and management of patients with renal artery stenosis: a cardiologic perspective. Prog Cardiovasc Dis 2003;46:271-286.

Renal artery stenosis is the most common cause of secondary hypertension. Over 90% of renal artery stenoses are caused by atherosclerosis, the remainder are caused by fibromuscular dysplasia (FMD).[ 1 ] Renal angioplasty is accepted widely as the treatment of choice for fibromuscular dysplastic disease potentially curing hypertension. [ 2 ] The situation is different for atherosclerotic renal artery disease, for which the treatment benefits are less clear, primarily because of increased patient age and significant comorbidity owing to generalized atherosclerosis. The complex interrelationship between atherosclerosis, renal artery stenosis, blood pressure, and renal function has been the subject of several recent reviews based on a variety of retrospective and prospective patient series and the combined clinical experience of many vascular surgeons, radiologists, general internists, and, more recently, invasive cardiologists. [ 1 , 3 , 4 , 5 , 6 and 7 ] On the one hand, renal angioplasty, particularly with stent implantation, technically is safe and effective, but on the other hand, there is little evidence from randomized controlled studies that renal revascularization is better than conservative management. At present, there are no uniform criteria on patient selection for conservative versus interventional treatment.

Renal artery stenting has replaced surgery as the standard treatment of renal artery stenosis.[ 8 ] Therefore, many patients have become eligible for renal revascularization who would not have been candidates for open surgical treatment because of their comorbidities. For example, a single center reported a dramatic increase of renal revascularizations from 4 per year to 57 per year within a 7-year period during which there was a switch toward endoluminal treatment. Although the procedural success rates were similar between the surgical and interventional treatment modalities, the former had a higher morbidity and mortality. [ 9 ]

There are 2 main groups of patients in whom renal artery stenosis should be considered (Table 1): young patients with new-onset hypertension and older patients with multiple cardiovascular risk factors with worsening of established hypertension and/or deterioration of renal function.

Fibromuscular dysplasia (FMD). Young patients with severe hypertension, typically women without cardiovascular risk factors, may have renal artery stenosis owing to FMD. FMD is a rare disorder of unknown cause. Nonostial segments of the renal artery are affected most often by FMD, but typical pathologic changes also may be seen in other visceral arteries. The FMD lesions are characterized by a focal thickening of the vascular wall and aneurysm formation, often resulting in a pathognomonic string of beads appearance at angiography. The diagnosis usually is made radiologically by the typical appearance of the vascular changes on selective angiography. Surgical correction rarely is necessary, thus the paucity of histologic material. Isolated lesions of FMD are amenable to angioplasty with good long-term results.[ 2 and 10 ] Younger patients with a relatively short history of hypertension may become normotensive without medication after renal angioplasty. The value of balloon angioplasty for fibromuscular dysplastic renal artery disease recently has been underscored by a prospective follow-up study of 27 patients with 31 treated renal artery stenoses in which 93% of patients had a cure or improvement of hypertension immediately after the procedure, which persisted in 74% of patients at 1 year. [ 10 ] Therefore, correction of the stenosis generally is indicated, although progression of the lesions to total occlusion and end-stage renal disease is rare. [ 1 ] FMD has been associated with cortical thinning in the ipsilateral kidney, [ 11 ] which also may be an indication for revascularization in patients with fibromuscular renal artery disease. [ 12 ]

Figure 1 Fibromuscular dysplasia of the right renal artery in a 29-year-old woman. A, Typical “string of beads” appearance with high grade stenosis. B, A successful angioplasty the stenosis is no longer visible and the control of blood pressure was improved.

The exact prevalence of renal artery stenosis in the general population is not known, but it is increasing with advancing age[ 13 ] and may be as high as 15% in autopsied patients who died of a stroke, [ 14 ] 25% diagnosed at coronary angiography, [ 15 ] or even almost 40% in patients undergoing angiography for aortic and peripheral vascular disease. [ 16 ] In contrast to fibromuscular dysplastic disease, progression of atherosclerotic renal artery stenosis is common and renal atrophy/complete occlusion may occur (rarely). [ 17 and 18 ]

Atherosclerotic renal artery stenosis is diagnosed with increasing frequency,[ 19 ] partly because of a reduced lethality of coronary artery disease owing to more effective treatment [ 20 and 21 ] and partly because of modern noninvasive diagnostic methods. Renal artery stenosis is a particularly relevant comorbid condition in cardiologic practice because risk factors for coronary artery disease and renal artery disease are identical. Consequently, around 25% of patients with coronary artery disease have some degree of renal artery stenosis, which may be hemodynamically relevant in up to 15%. [ 15 and 22 ]

From a practical clinical standpoint, renal artery disease and coronary heart disease are interrelated in several ways: renal artery stenosis may contribute to hypertension and/or interfere with its treatment. Renal artery stenosis therefore has a negative impact on both primary and secondary prevention of coronary events. Indeed, renal artery stenosis is a strong negative prognostic indicator for cardiovascular events: the mortality of patients with coronary artery disease and renal artery stenosis is doubled compared with patients undergoing cardiac catheterization without renal artery disease; moreover, survival was correlated inversely with the severity of the renal artery stenosis.[ 23 and 24 ]

Recurrent flash pulmonary edema despite a good left ventricular function is another indicator of significant renal artery stenosis. This clinical syndrome of apparent heart failure can be caused by severe bilateral renal artery stenosis or a critically stenosed artery to a single functioning kidney. Because of the compromised renal perfusion, the increase in blood pressure is not accompanied by a commensurate pressure natriuresis. Therefore, a hypertensive crisis may develop, leading to pronounced diastolic dysfunction and pulmonary edema. Correction of the stenosis can result in an increased excretion of sodium and prevents recurrence of the pulmonary edema.[ 25 and 26 ] It has been suggested that these patients with volume retention owing to bilateral renal artery stenosis or unilateral stenosis to a single functioning kidney may derive the greatest benefit from renal revascularization. [ 27 ]

Patients with congestive heart failure who develop acute renal failure on angiotensin-converting enzyme (ACE) inhibitors are another group in whom renal revascularization should be considered. These patients may have (bilateral) renal artery stenosis or stenosis to a single functioning kidney. ACE inhibitors are the afterload reducing agents of choice in patients with heart failure in whom they provide a prognostic benefit. Renal revascularization may allow subsequent treatment with ACE inhibitors.

Renal artery stenosis is an increasingly important cause of end-stage renal disease, especially in the elderly.[ 28 and 29 ] Therefore, it can be worthwhile to offer the evaluation of renal artery stenosis/renal angioplasty to selected patients (relatively preserved kidney size) entering dialysis programs because there are several anecdotal reports of sufficient recovery of renal function after renal revascularization to discontinue dialysis. [ 30 and 31 ]

The kidney plays a central role in the regulation of blood pressure. The importance of the renin-angiotensin-aldosterone system for the generation of the hypertension is well recognized. However, the mechanisms of the hypertension in patients with renal artery stenosis are complex because not all patients with renovascular disease, especially not with atherosclerotic renal artery stenosis, have (renin-dependent) renovascular hypertension.[ 7 ] In patients with severe bilateral renal artery disease or stenosis of a single functioning kidney, volume overload with secondary suppression/normalization of the plasma renin activity is an important mechanism for the maintenance of the hypertension. Another important mechanism is renal parenchymal hypertension owing to hypertensive nephrosclerosis, renal hypoperfusion owing to congestive heart failure, atheroembolic disease, diabetes mellitus, and so forth. There is considerable overlap between renovascular and renoparenchymal hypertension in patients with atherosclerotic renal artery stenosis, which may be coincidental to the hypertension rather than causal. [ 32 ]

When the renal perfusion pressure is decreased such as downstream of a hemodynamically relevant renal artery stenosis intrarenal compensatory mechanisms are activated to maintain the glomerular filtration rate (GFR) despite the reduced perfusion. This intrarenal counterregulation is characterized by an increased filtration fraction through the constriction of the efferent arteriole of each glomerulum while the afferent arteriole is dilated. The efferent arteriolar constriction is mediated by angiotensin II, whereas the afferent arteriolar dilatation is mediated by vasodilatory prostaglandins. These regulatory mechanisms of the glomerular hemodynamics explain the increased risk for acute renal failure owing to the administration of ACE inhibitors (and angiotensin receptor blockers, although there are fewer published data) and/or nonsteroidal anti-inflammatory drugs in these patients. The administration of an ACE inhibitor blocks the angiotensin II effect on the efferent arteriole and causes a precipitous decrease in the GFR. This drop in the GFR may not be apparent clinically if the nonstenotic contralateral kidney can compensate the reduction of GFR in the poststenotic kidney.

In addition to the renin-angiotensin-aldosterone system, several other mechanisms contribute to the pathogenesis of hypertension in renal artery stenosis including the sympathetic nervous system,[ 33 and 34 ] nitric oxide, [ 35 and 36 ] and endothelin. [ 37 and 38 ] The relative importance of the different systems is not clear. There is experimental evidence that oxidative stress is increased in renovascular hypertension. [ 39 ] Oxidative stress contributes to the pathogenesis of atherosclerosis [ 40 ] and could therefore accelerate the progression of atherosclerotic lesions not only in the kidney (positive feedback loop), but also in the heart and in other organs. This may explain why renal artery stenosis is a negative prognostic factor in atherosclerotic cardiovascular disease. [ 24 ] Recently it has been reported that renal revascularization can reduce oxidative stress and endothelial dysfunction in patients with renal artery stenosis, [ 41 ] suggesting that prognostic improvement may be possible.

The diagnostic evaluation of renal artery stenosis is indicated in patients who are candidates for renal revascularization as outlined in Table 2 . A high index of suspicion is usually the key element of diagnosis. Physical examination mostly is not helpful, but in some patients an abdominal or flank bruit may be a diagnostic clue. Because patients with renal artery stenosis may have hyperreninemic hyperaldosteronism as a feature of renovascular hypertension, hypokalemia can be present. The urinalysis may show nonspecific proteinuria and other changes of chronic renal insufficiency.

A clinical prediction rule can have a sensitivity of 72% and a specificity of 90% in selecting patients for angiography,[ 42 ] which is the current gold standard for the diagnosis of renal artery stenosis. In general clinical practice, usually a combination of functional and imaging studies are used to diagnose renal artery stenosis. The sensitivity and specificity of commonly used noninvasive tests such as captopril renal scintigraphy and systemic renin measurements are inferior to other noninvasive techniques that more recently have become available. [ 43 ] Moreover, renal scintigraphy provides no anatomic information and has a limited diagnostic accuracy. [ 44 ] On the other hand, (captopril) renal scintigraphy is not as investigator dependent as duplex ultrasonography and may be informative in patients who are not suitable for duplex ultrasound or magnetic resonance angiography. In addition, renal scintigraphy is a useful method to measure unilateral renal function and to estimate the functional significance of an intermediate stenosis. Exercise renal scintigraphy has been proposed as a noninvasive tool to distinguish between patients with essential hypertension and renovascular hypertension and to help in patient selection for renal revascularization, [ 45 ] but this test is not routinely available.

In many centers magnetic resonance angiography rapidly is becoming the method of choice for the diagnosis of renal artery stenosis because it is noninvasive and avoids iodinated radiocontrast agents.[ 46 and 47 ] In addition to delineating the renal arterial anatomy, this technique allows the measurement of renal function and perfusion, which can reflect the hemodynamic relevance of renal artery stenosis. [ 48 and 49 ] However, the (patho-) physiologic interpretation of the angiographic picture is not without pitfalls [ 47 ] and the technique requires experienced radiologists to avoid the overestimation of the severity of the stenosis.

Duplex ultrasonography usually is combined with conventional renal ultrasound, which provides valuable indirect clues as to the presence of renal artery stenosis and may help with patient selection for revascularization. Renal atrophy is irreversible. Therefore, no significant functional improvement can be expected in small kidneys and it has been proposed that renal artery stenosis in kidneys less than 7.5 cm should be managed conservatively.[ 4 ] Very rarely an atrophied kidney can maintain hypertension. However, owing to the efficacy of modern antihypertensive drugs, nephrectomy for control of hypertension is all but obsolete.

Arterial digital subtraction angiography (DSA) is still the gold standard for the detection and morphologic delineation of renal artery stenosis. Earlier radiologic techniques such as venous DSA or rapid sequence excretion pyelography are obsolete. A flush abdominal aortic angiogram, preferably in an oblique projection, may suffice to show a significant renal artery stenosis, but it cannot exclude the diagnosis because tight ostial lesions may be concealed.

Detailed anatomic information is the precondition for renal revascularization. The percutaneous revascularization can be performed in the same session if clinical assessment and/or noninvasive methods have increased the pretest probability of the presence of a clinically significant renal artery stenosis and the patient has given informed consent. Therefore, the invasive and noninvasive diagnostic methods are not redundant, but rather complementary. In the rare patient in whom the results of the noninvasive tests are not in agreement with the morphologic severity of the stenosis, direct measurement of the pressure gradient proximal and distal to the stenosis may be useful in deciding whether or not to proceed with angioplasty. Because arterial DSA requires cannulation of the aorta and exposes the patient to potentially nephrotoxic radiocontrast agents, this invasive procedure should be reserved for patients in whom renal revascularization is considered. Patients with atherosclerotic renal artery stenosis often have chronic renal insufficiency and are therefore at increased risk for radiocontrast-induced nephropathy .[ 55 ] Carbon dioxide can be used as an alternative, noniodinated contrasting agent, especially for interventional applications. [ 56 ] Alternatively, nonnephrotoxic paramagnetic contrast agents used in magnetic resonance angiography may be useful. [ 57 ]

Even without nephrotoxic radiocontrast agents the cannulation of the aorta and renal arteries carries renal risks. This is true especially in patients with atheromatous degeneration of the aorta and/or atherosclerotic aneurysms in whom intraluminal catheter manipulations can dislodge thrombi or plaque causing downstream microembolization of plaque fragments. Because of their large blood supply (some 20% of the cardiac output) the kidneys often are affected by cholesterol embolization syndrome , which can cause irreversible renal dysfunction and even end-stage renal disease.[ 58 ]

About a quarter of patients undergoing coronary angiography have some degree of renal artery stenosis. The risk for renal artery stenosis corresponds with the severity of the coronary artery disease and with reduced renal function, diabetes mellitus, and systolic hypertension.[ 59 and 60 ] Therefore, it may be efficient to perform renal arteriography as part of the coronary procedure with little additional risk provided the total amount of radiocontrast is limited. [ 61 ] Not all hypertensive patients with morphologic evidence of renal artery stenosis benefit from angioplasty. Therefore, the imaging of the renal arteries during coronary angiography in all hypertensive patients as a screening measure is not recommended. However, it seems reasonable to have a low threshold for offering renal angiography as part of a coronary procedure to patients with a high pretest probability of having renal artery stenosis on clinical grounds and/or from the results of noninvasive testing. [ 62 ]

Recognizing and treating renal artery disease in patients with coronary artery lesions can be particularly rewarding because of the close functional and clinical interrelationship of the 2 organs. Improving renal perfusion may influence the course of cardiac disease because renal dysfunction has a major impact on cardiac mortality.[ 63 ] Moreover, renal failure worsens the outcome of coronary artery bypass grafting [ 64 ] and percutaneous coronary interventions. [ 65 , 66 and 67 ]

Not all patients with renal artery stenosis require renal revascularization. The recent Dutch Renal Artery Stenosis Intervention Cooperative Study (DRASTIC) was a carefully conducted, multicenter, randomized, controlled trial on 106 patients with atherosclerotic renal artery stenosis. After 12 months of follow-up there was no difference in systolic or diastolic blood pressure between the angioplasty and conservatively treated group. Therefore, angioplasty may offer little advantage over antihypertensive drug therapy.[ 68 ] However, 22 patients crossed over from the conservatively treated group into the angioplasty group after randomization and only 2 patients received an intravascular stent. Hence, this study is not representative for the current clinical preference to stent ostial renal artery lesions.

Preservation of renal function has not been shown in randomized controlled trials. However, the conservative management of patients with azotemic renovascular disease and severe hypertension is problematic because any medication that is effective in lowering blood pressure is liable to worsen renal function.[ 69 ] This is particularly true for drugs that inhibit the renin-angiotensin system because of their specific effects on the regulation of the GFR. ACE inhibitors can induce a deterioration of renal function in patients with high-grade renal artery stenosis to a single-function kidney or in severe bilateral disease. [ 70 ] On the other hand, ACE inhibitors are highly effective in the treatment of renovascular hypertension, particularly when combined with a diuretic, and do not necessarily induce renal atrophy or azotemia even if mild renal insufficiency is present at the start of therapy. [ 71 ] It is a misconception that these highly effective agents are sometimes viewed as contraindicated in patients with renal artery stenosis. On the contrary, they are rather the treatment of choice except in patients who develop rapidly worsening azotemia, which is usually readily reversible on discontinuation of the offending drug. By extrapolation, the same should apply for angiotensin II antagonists, although there are still fewer published data. Monitoring renal size and (unilateral) function is advisable to detect atrophy of the poststenotic kidney under ACE inhibition. This may be an indication to proceed with revascularization of the stenotic kidney, but in many clinical settings this may be tolerated because experiments in rats suggest that the reduction or even loss of function of the poststenotic kidney is overcompensated by the beneficial effect of ACE inhibition on the contralateral kidney resulting in a stable or even improved overall renal function and better survival. [ 72 ] Hence, with careful follow-up, patients with renal artery stenosis can be managed conservatively provided the hypertension is controlled on medications and renal function remains stable. [ 4 ]

There are several clinical criteria that may help in patient selection for conservative versus interventional treatment. The characteristics of patients in whom conservative management is favored are given in Table 2 . If patients respond to antihypertensive treatment and the renal function does not deteriorate, it is reasonable to continue drug treatment with monitoring of blood pressure and renal function. Because the sympathetic nervous system is activated in renovascular hypertension, [ 34 ] β-blockers usually are indicated.

Patients with renal artery stenosis have a particularly high atherosclerotic cardiovascular risk.[ 23 ] Therefore, they should receive aggressive secondary prevention measures, including aspirin and statins. In addition to reducing cardiovascular risk by lowering cholesterol, the latter have pleiotropic effects including the reduction of oxidative stress, which has been shown to be increased in renovascular hypertension. [ 39 and 73 ] It has been suggested that meticulous secondary prevention may ameliorate the course of renal artery stenosis and improve clinical outcomes. [ 74 ]

The most common anatomic location of atherosclerotic renal artery stenosis is the aortic ostium. This may be owing to turbulent blood flow at the renal artery ostium because of the high renal blood flow (some 20% of cardiac output) and possibly the angle of the renal artery origin. Turbulent flow increases the risk for endothelial injury at this location, which could be the focus of atherosclerotic plaque formation. It is not uncommon for both renal artery orifices to be narrowed by atherosclerotic plaque.[ 75 ] The results of balloon angioplasty of these atherosclerotic ostial renal artery lesions are not satisfactory. [ 76 and 77 ] The outcome of ostial renal artery intervention has been improved dramatically by combining angioplasty with stent implantation of the renal artery ostium. This can be accomplished without a guiding catheter when the balloon is advanced over a relatively stiff guidewire and visualization of the renal artery ostia is achieved using a separate catheter introduced via the contralateral femoral artery. [ 78 ] More recently several guiding catheters and stent delivery systems have been developed that are adaptations from the percutaneous transluminal coronary angioplasty (PTCA) equipment familiar to interventional cardiologists. We generally use a 6 or 7 F Judkins guiding catheter for the right coronary artery or for the internal mammary artery with sideholes to minimize renal hypoperfusion when engaging tight ostial lesions. This technique allows the use of atraumatic 0.018′ steerable guidewires that are used in coronary revascularization. By using the guiding catheter/over the wire (rapid exchange) technique the balloon can be advanced under direct vision over the thin PTCA guidewire, thus minimizing the risk for renal parenchymal injury caused by inadvertent advancement of the guidewire during the procedure. [ 79 ]

A multitude of studies and reports on renal angioplasty with stent implantation have been published ( Table 3 , Table 4 and Table 5 ). The subject also has been reviewed extensively.[ 3 , 6 , 80 and 81 ] The largest published, single-center series with 363 renal artery stenoses in 300 patients showed a technical success rate of 100% without procedural deaths or emergency surgical procedures and an overall re-stenosis rate of 21%, retrospectively 12% in renal arteries with a diameter greater than 4.5 mm. [ 82 ] These excellent results make primary renal artery stenting an attractive treatment option and explain why renal artery angioplasty with stenting has largely replaced surgical revascularization as the treatment of choice for atherosclerotic renal artery stenosis, especially because surgical treatment is accompanied by a higher morbidity and mortality. [ 9 ] Renal artery stenting is also safe and effective in patients with increased renal risk owing to a single functioning native [ 83 and 84 ] or transplanted [ 85 and 86 ] kidney.

Distal renal embolization of plaque material is a concern with renal artery angioplasty, especially when predilatation is necessary before stent implantation. This problem may be circumvented using a distal protection device,[ 87 ] but currently this technique is not standard practice.

Figure 2 shows an example of an 82-year-old woman with refractory severe hypertension and chronic renal insufficiency (serum creatinine concentration 1.6 mg/dL), 2 high-grade stenoses of the left renal artery (ostium and siphon-like midportion) were treated successfully with angioplasty and the implantation of 2 stents in the same session using a modified PTCA technique. After a transient increase of the serum creatinine concentration to a peak of 3.0 mg/dL, during which the patient was not oliguric, the serum creatinine concentration gradually returned to baseline. There was a marked improvement in blood pressure control after renal revascularization documented by 24-hour ambulatory blood pressure recording despite a reduction of the antihypertensive medication.

The risk for acute renal artery stent thrombosis is low, possibly owing to the high renal arterial blood flow. To our knowledge there are no published randomized studies on stent patency comparing different antiplatelet and/or anticoagulation regimens. In the absence of evidence-based information for the renal artery, we inhibit platelet function after renal artery stent implantation with aspirin (100 mg/d) and clopidogrel (75 mg/d for 4 wk) analogous to our patients with intracoronary stents.

The long-term results of renal artery stenting generally are good, but the problem of restenosis does exist ( Table 3 and Table 4 ) and may be up to 37%. [ 88 ] The rate of restenosis is not established as clearly as in the coronary circulation because the follow-up in the published patient series has been variable and sometimes included only patients without duplex sonographic evidence of restenosis at 1 year. [ 89 ] Restenosis can be treated with repeat angioplasty with or without stent implantation with a 75% success rate and stable renal function at 1 year. [ 90 ] In patients with recurrent restenosis, brachytherapy is feasible, [ 91 ] but will likely be superceded in the near future by antiproliferative drug-eluting stents that already are being used in the coronary circulation and may soon become available for extracardiac applications.

Table 3 and Table 4 give an overview on some of the larger retrospective (the majority with renal artery stenting) and prospective reports on percutaneous renal revascularization during the past 5 years. Only patient series that had greater than 25 patients were included. It is clear that renal artery stenting is angiographically very effective with a low acute complication rate. The various patient series are very heterogeneous, but the compiled results suggest an overall modest benefit on blood pressure and no clear benefit on renal function. This is consistent with an earlier review of renal artery stenting in 10 studies [ 92 ] and with 2 recent meta-analyses of the 3 randomized controlled trials in this field that are summarized in Table 5 (see later). [ 93 and 94 ] These 3 randomized studies were designed primarily to test the effect of renal angioplasty on blood pressure. There is still no published information from randomized controlled trials regarding the effect of renal angioplasty on renal function or on hard endpoints such as (total) mortality or end-stage renal disease.

There are 2 arguments for renal revascularization: blood pressure control and preservation/improvement of renal function. In the following paragraphs the outcomes of renal revascularization on these 2 indications are considered separately.

Although renal revascularization is unlikely to cure hypertension in patients with atherosclerotic renal artery disease, the blood pressure is better controlled and/or requires fewer antihypertensive medications after successful angioplasty ( Table 3 , Table 4 and Table 5 ). This pertains to the number of different medications, as well as to their total daily dose. This is consistent with the earlier surgical experience that renal revascularization in patients with atherosclerotic renal artery disease helps to achieve better control of blood pressure on fewer medications. [ 95 ]

The indication for renal artery intervention for blood pressure control recently has been challenged in view of the results from randomized studies ( Table 5 ). A randomized study comparing medical therapy with angioplasty in 55 patients with atheromatous renal artery stenosis showed a mild improvement of blood pressure control only in patients with bilateral disease without improvement in renal function, but at a significant complication rate. [ 96 ] The larger DRASTIC trial published by van Jaarsveld et al [ 68 ] suggested that angioplasty offers little advantage over antihypertensive drug therapy. Another randomized controlled trial of angioplasty versus conservative treatment on 49 patients showed no significant reduction in ambulatory blood pressure, but a reduction in medication requirement. [ 97 ] These 3 randomized controlled trials were combined and collectively evaluated in 2 meta-analyses that were published earlier this year. [ 93 and 94 ] The conclusion of Nordman et al [ 93 ] pointed to a modest effect on blood pressure control; an effect on renal function was not determined because none of the studies were designed to analyze this. Ives et al [ 94 ] concluded that the 3 randomized trials each were too small to evaluate the effect of angioplasty in atherosclerotic renovascular disease. However, the combination of the 3 trials in their meta-analysis failed to show a large benefit with respect to hypertension or renal function, but a smaller yet clinically significant benefit could not be excluded. They conclude that further, large-scale, randomized studies are needed to address this possibility.

The preservation/improvement of renal function has become an increasingly important indication for renal revascularization because the control of blood pressure often can be achieved with modern antihypertensive drugs.[ 98 ] Although less than 10% of patients with renal artery stenosis develop progressive renal failure, [ 99 ] ischemic nephropathy is the fastest growing cause of end-stage renal disease in the United States, [ 19 ] accounting for 11% to 14% of cases [ 29 ]; in a recent European report it was the most common cause of end-stage renal disease in the elderly. [ 28 ]

The renal function outcome of atherosclerotic renal artery stenting is a complex issue. In addition to the general risks of invasive arterial procedures, renal interventions carry a significant renal risk, mainly related to radiocontrast nephropathy and/or cholesterol embolization from atheromatous plaques. Hence, it is not surprising that renal function does not uniformly improve after successful revascularization and may even deteriorate in some patients. There are no published, randomized, controlled studies designed to evaluate outcome of conservative management versus renal artery stenting on renal function. The 3 randomized controlled renal artery stenting/blood pressure trials that were evaluated in the recent meta-analyses failed to show a benefit on renal function; however, none of the trials was designed to study renal function outcomes.[ 93 and 94 ] Because many of the patients with renal artery stenosis are elderly and have a reduced muscle mass, the serum concentration of creatinine may be misleading as a surrogate marker for renal function. Future studies should be based on more accurate assessments of the GFR either by direct clearance measurements or at least by reporting an estimation of GFR taking into account age and lean body weight. [ 100 ]

A compilation of 10 descriptive studies of the effect of renal artery stenting on the serum creatinine concentration showed an equal rate of improvement and deterioration of renal function (each 26% of patients), whereas in the majority of patients (48%) there was no change in the serum creatinine concentration.[ 92 ] These figures are remarkably similar to the early preliminary study reported by Rees et al [ 101 ] and to the results from the single-center series reported by Lederman et al. [ 82 ] The renal function improved in 19% of patients with renal insufficiency before the intervention. This is in contrast to a decrease of renal function in 27% of patients. In the remainder (54%), there was no change in renal function before and after the procedure, indicating that the improvement of renal perfusion had no effect on renal function in the majority of patients.

Patients who stand to gain the greatest benefit from renal revascularization also may have the highest risk of suffering from the procedure. This applies to radiocontrast nephropathy, the risk of which is increased greatly in proportion to the degree of renal dysfunction. It is also true for patients with diffuse atheromatosis, who have an increased risk for cholesterol embolization. Therefore, the functional outcome of renal artery stenting is largely unpredictable in individual patients, although modern techniques of risk stratification may be helpful.[ 54 and 102 ]

Watson et al[ 103 ] published their experience of renal artery stenting in 33 patients with deteriorating renal function. During 20 ± 11 months of follow-up, renal function improved and/or the deterioration of renal function was halted in all patients, which was reflected by a preservation of renal size. Patients with declining renal function benefited from renal artery stenting in another prospective report on 63 patients with renal insufficiency. [ 104 ] On the other hand, despite stent implantation 5 patients reached end-stage renal failure within 6 months and patients with stable renal function did not seem to benefit. Thus, renal revascularization appears to be most beneficial in patients with deteriorating renal function, but the procedure itself may be harmful and its overall effect on patients with atherosclerotic renal artery disease remains to be determined. Hence, careful patient selection and informed consent are important. The situation may be different in patients with terminal renal failure already on renal replacement therapy. Because these patients have little renal function to lose, the clinical relevance of the renal function risk of renal revascularization is limited. This may argue in favor of a trial of a salvage angioplasty in patients with relatively preserved renal size/parenchymal thickness on ultrasound and recent-onset end-stage renal disease because there are several anecdotal reports of patients coming off dialysis after renal revascularization. [ 30 and 31 ]

Overall it can be summarized that the evidence for improved blood pressure control after renal revascularization is somewhat stronger than for preservation/amelioration of renal function. However, in clinical practice blood pressure often can be controlled pharmacologically, whereas there are no practical alternatives to renal revascularization for the purpose of improving or preserving renal function. Given the lack of conservative treatment options to improve renal function in these patients there is a real need for evidence-based information from randomized controlled trials on the renal function outcome of renal artery stenting. It is doubtful if this information ever will become available because a large number of patients are likely to die from their cardiovascular comorbidity before any long-term benefit on renal function can be ascertained statistically.

The angiographic outcome of renal artery stenting is good and the procedure is safe, especially when using a modified PTCA technique. The control of blood pressure is improved, but the clinical benefit of the mostly modest improvement has not been shown unequivocally. The outcome of renal angioplasty on renal function is less certain: the chance of an amelioration of renal function is counterbalanced by the risk for (worsening) renal failure. It is difficult to predict the risk-benefit ratio in individual patients, although the renal resistance index and some clinical parameters may be helpful for patient selection. In most patients renal revascularization is inconsequential for renal function. In appropriately selected patients, diagnosing renal artery stenosis may be cost effective.[ 105 ]

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