doi: 10.1161/CIRCULATIONAHA.106.619015
(Circulation. 2007;115:263-270.)
© 2007 American Heart Association, Inc.
Controversies in Cardiovascular Medicine |
Is renal artery stenting the correct treatment of renal artery stenosis? The Case for Renal Artery Stenting for Treatment of Renal Artery Stenosis
From the Department of Medicine, University of Toledo, Toledo (C.J.C.), and Department of Diagnostic Imaging, Brown University, Vascular Disease Research Center, Rhode Island Hospital, Providence (T.P.M.).
Correspondence to Christopher J. Cooper, MD, Department of Medicine, University of Toledo, 3000 Arlington Ave, Hospital Room No. 1192, Toledo, OH 43614–2598. E-mail ccooper{at}mco.edu
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Introduction |
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 Top Introduction RAS and HypertensionRAS and Kidney FunctionRAS and Cardiovascular EventsLimitations of Medical Therapy...Intervention Cohort StudiesLimitations of Nonrandomized...How Should Patients Be...ConclusionsReferences |
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The case favoring renal artery stenting for individuals with renal artery hypertension is largely circumstantial. At best, the clinical evidence presented in this discussion is derived primarily from nonrandomized cohort studies. It would certainly be easier to argue that medical therapy is preferred for such individuals because there are 3 published randomized clinical trials that concluded just that and none that support renal artery intervention. Nonetheless, there is considerable evidence to support the role for revascularization in general, and stenting specifically, as an important adjunctive therapy to medical therapy in the care of patients with renal artery stenosis (RAS). The argument has 3 principal components: observations about the impact on cardiovascular physiology, end-organ effects, and natural history.
Response by Dworkin and Jamerson p 270
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RAS and Hypertension |
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TopIntroductionRAS and HypertensionRAS and Kidney FunctionRAS and Cardiovascular EventsLimitations of Medical Therapy...Intervention Cohort StudiesLimitations of Nonrandomized...How Should Patients Be...ConclusionsReferences |
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RAS is associated with and is an important cause of secondary hypertension. RAS causes endocrine activation with release of renin from renal juxtaglomerular cells. Renin catalyzes the breakdown of angiotensinogen to angiotensin I. Angiotensin I is transformed by angiotensin-converting enzyme into angiotensin II, and angiotensin II promotes the release of aldosterone from the adrenal cortex.1 Angiotensin II is a potent vasoconstrictor,2 substantially more potent than epinephrine, and is implicated in end-organ damage in the heart3 and kidney.4 RAS is suggested to cause 2 types of hypertension. With unilateral RAS and a normally perfused and normally functioning contralateral kidney, blood pressure elevation is referred to as "renin dependent" and is characterized by increased peripheral resistance.5,6 In this circumstance, renin and angiotensin levels remain elevated, but volume expansion is limited by natriuresis of the contralateral normally functioning kidney.6 Importantly, although renin levels are elevated, the value of peripheral or even renal vein renin values is limited by substantial overlap with patients having essential hypertension.7,8
When stenoses are bilateral or when the contralateral kidney is absent or is dysfunctional, intravascular volume increases and renin secretion decreases over a period of 5 to 10 days.6,9–13 Without the natriuretic effect of a normally perfused contralateral kidney, hypertension is maintained by volume expansion. This scenario is described as 1-kidney 1-clip Goldblatt hypertension.
In addition, the sympathetic and central nervous systems contribute to hypertension in RAS.14–16 RAS also causes increased production of vasoactive reactive oxygen species, which increases vasomotor tone.17 Ischemic injury of the affected kidney(s), hypertensive nephrosclerosis of the contralateral kidney, or hypertrophy of the peripheral vasculature also may be important contributors to sustained hypertension with RAS.6 Abnormal endothelium-dependent vasodilation also appears to be found and may be associated with increased oxidative stress.17 Recent work suggests that primary hyperaldosteronism may contribute to the persistence of hypertension in a significant minority of patients who appear to be unresponsive to revascularization.18
Thus, it is clear that hypertension is an important consequence of RAS. Antihypertensive medical therapy may address one or several of these mechanisms, but revascularization with endovascular stenting may be an efficient mechanism to downregulate many of these changes.15,17 As an example, successful renal artery revascularization may decrease muscle sympathetic nerve activity,15 as does denervation of the affected kidney,19 and may improve endothelial function.17,20
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RAS and Kidney Function |
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TopIntroductionRAS and HypertensionRAS and Kidney FunctionRAS and Cardiovascular EventsLimitations of Medical Therapy...Intervention Cohort StudiesLimitations of Nonrandomized...How Should Patients Be...ConclusionsReferences |
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Although end-stage renal disease is uncommon in the short term,21 historical data suggest that up to 27% of those with RAS develop chronic renal failure within 6 years.22 Importantly, several investigators have reported that renal artery revascularization is associated with stabilization or improvement in renal function.23–26
The adverse effect of ischemia on the kidney is well established experimentally and clinically. The role of atherosclerotic RAS in the genesis of renal dysfunction is controversial, however. Over 1 to 4 years, atherosclerotic stenoses often progress, some to occlusion.22,27–29 RAS is associated with loss of renal size, a reasonable but crude measure of renal function.29 In patients with significant (>60%) RAS, 1 of 4 ipsilateral kidneys demonstrates atrophy of >1 cm in length,30,31 whereas significant loss of renal size is uncommon without RAS.30 Occlusion is associated with substantial loss of renal size and function.32
Several investigators have been unable to demonstrate a relationship between stenosis severity and renal function.33,34 Although one might conclude from this finding that stenoses do not cause renal dysfunction, such a conclusion would be unfounded. Fundamentally, the kidney requires blood flow to function. Clearly, there are factors beyond percent stenosis that influence function. Some are intrinsic to RAS, including the duration of the insult, atheroemboli, hypertensive nephrosclerosis of the contralateral kidney, activation of the renin-angiotensin system, and effect of the stenosis (including lesion length, minimal lumen diameter, etc) on renal blood flow and intrarenal pressure. Additionally, other factors such as essential hypertension, diabetes, concomitant medications, generalized atherosclerosis progression, and aging play a role in determining overall renal function.
Most research has ascribed a direct role of the renin- angiotensin system in ischemic nephropathy. Angiotensin II induces efferent arteriolar constriction, which aids in the maintenance of glomerular filtration rate. Kidneys remain viable with blood flows and pressures below that required for glomerular filtration because <10% of oxygen delivery is required for kidney tissue metabolism.35 Thus, chronic ischemia does not damage renal tissue simply by lack of oxygen delivery.36 Chronic renal failure can be the result of severe global ischemia, but nephrosclerosis also occurs in the nonstenotic kidney, perhaps mediated by hypertension, a vasculotoxic effect of renin,37,38 or by angiotensin II through its interaction with endothelin-1, platelet-derived growth factor-ß, and transforming growth factor-ß.4 Gobe et al39 studied the cellular events related to unilateral RAS when the kidney underwent progressive atrophy. During the initial phase (2 to 5 days), tubular cell death resulted from both necrosis and apoptosis. During the later phase (10 to 20 days), renal atrophy progressed, and cell death resulted from apoptosis alone. After reversal of RAS, evidence of regeneration, consisting of hypertrophy and hyperplasia, was found. These findings imply that chronic ischemia is a dynamic process comprising not only an adaptation to reduced blood flow but also a potential for tubular cell regeneration.
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RAS and Cardiovascular Events |
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TopIntroductionRAS and HypertensionRAS and Kidney FunctionRAS and Cardiovascular EventsLimitations of Medical Therapy...Intervention Cohort StudiesLimitations of Nonrandomized...How Should Patients Be...ConclusionsReferences |
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In patients with RAS, the risk of cardiovascular morbidity and mortality appears to be substantial. Wollenweber et al22 described a 6-year cardiovascular event–free survival of 53%, with risk related to the severity of the renal stenosis. Several others have suggested that the risk of adverse cardiovascular events is high and occurs in excess of the severity of hypertension.40–42 More recently, a significant decrease in 4-year survival was seen in patients with incidental RAS undergoing coronary angiography.43 Thus, the risk of cardiovascular events appears to be high in RAS, and blood pressure control may be a poor surrogate for clinical outcomes.
It is not known whether the high cardiovascular event rate seen in patients with atherosclerotic RAS is attributable to the effects of renal ischemia and subsequent neuroendocrine activation or is simply a marker for advanced atherosclerosis and cardiovascular risk. A biologically plausible link is present, however, between renal ischemia and subsequent events that may be independent of blood pressure per se. Angiotensin II is implicated in smooth muscle proliferation, plaque rupture, endothelial dysfunction, and inhibition of fibrinolysis.3 Angiotensin II also promotes medial and cardiac myocyte hypertrophy.6,44–51 It is important to note that myocardial hypertrophy occurs when angiotensin II is present even when blood pressure is controlled.52 Angiotensin II interacts with other peptides like endothelin, transforming growth factor-ß, and platelet-derived growth factor-ß, each of which is implicated in end-organ damage, ventricular hypertrophy, and vascular hypertrophy.4,51–53 Excess aldosterone has been related to extracellular matrix and collagen deposition and therefore to myocardial fibrosis.54
Although the mechanism(s) responsible for the relationship between RAS and congestive heart failure (CHF) are not well characterized, there is little doubt that ventricular hypertrophy, sustained hypertension, activation of the renin-angiotensin and sympathetic nervous systems, and volume retention associated with renal ischemia are likely important contributors. Recent work suggests a relationship between brain natriuretic peptide and RAS, with high brain natriuretic peptide levels (>80 pg/mL) associated with better outcomes after renal artery intervention.55 Angiotensin II, endothelin, or an insulin-like growth factor, and sympathetic activation all may be involved in the process of ventricular thickening and stiffening.46–49,53 Angiotensin has been implicated in the mechanism of cardiac hypertrophy and is known to induce protein synthesis in myocardial cells,50 even when the mean arterial pressure is lowered.52 Endothelin also has been implicated in cardiac hypertrophy in RAS.51 Interestingly, the use of endothelin receptor blockers reverses left ventricular hypertrophy in rats with RAS.48,51
Remodeling of the left ventricular wall and peripheral arteries in response to renovascular hypertension has been noted. In patients with RAS with hypertension, cardiac remodeling permits maintenance of normal cardiac function despite increased left ventricular wall stress resulting from systemic hypertension.56 Ventricular performance, determined by afterload, chamber size, mass index, and functional shortening or contractility, often is abnormal in people with renovascular hypertension.5,57
Congestive heart failure is common in patients undergoing renal artery revascularization,58–60 just as RAS is common in patients presenting with CHF.61 Left ventricular hypertrophy and decreased contractility, risk factors for development of overt CHF,62 are significantly more common in those with renovascular hypertension than essential hypertension,44,63 even when matched for age and gender.5 RAS is prevalent in those with CHF and may be implicated in its cause or severity in a large proportion of patients. In a series of patients >70 years of age presenting with New York Heart Association class II to IV heart failure, 34% were found to have stenosis of at least 50% involving at least 1 renal artery.61
As discussed, left ventricular hypertrophy is an important risk factor for cardiovascular events and cardiovascular death in both the presence and absence of hypertension.64–71 Regression of left ventricular hypertrophy is favorable prognostically,69 and left ventricular mass index, a measure of ventricular hypertrophy, has been shown to decrease after renal artery revascularization.72 When CHF accompanies RAS, renal artery revascularization often is associated with symptomatic improvement.60,73 Currently, this may be underrecognized in clinical practice. There certainly appears to be some confusion about the management of patients with RAS and CHF; the recent American Heart Association/American College of Cardiology consensus document on the management of peripheral vascular disease74 suggests limited support for screening patients with CHF but substantial support for treatment of RAS in patients with CHF, despite a paucity of evidence to support either position.
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Limitations of Medical Therapy for RAS |
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TopIntroductionRAS and HypertensionRAS and Kidney FunctionRAS and Cardiovascular EventsLimitations of Medical Therapy...Intervention Cohort StudiesLimitations of Nonrandomized...How Should Patients Be...ConclusionsReferences |
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Undoubtedly, all patients that have RAS require lifelong medical therapy to manage the underlying atherosclerotic process with statins, antiplatelet therapy, antihypertensive therapies, and hypoglycemic agents in the presence of diabetes. Inhibition of sympathetic activation and the renin-angiotensin-aldosterone system with ß-blockers and angiotensin-converting enzyme inhibitors is a very successful strategy for patients with cardiovascular diseases in several settings, including acute myocardial infarction, CHF, and hypertension. In each of these settings, treatment has demonstrated significant benefits as measured by reductions in clinically important events. Renin-angiotensin-aldosterone system–inhibiting drugs also are indicated for retarding the progression to end-stage renal disease to preserve renal function.75,76 Although there are no outcome data with antihypertensive medical therapy for treatment of RAS specifically, clinical studies suggest that renin-angiotensin-aldosterone system inhibition decreases cardiovascular events in other high-risk patient groups.77,78
Antihypertensive medical therapies can be associated with adverse health effects, however, such as lack of energy or chronic cough, which may affect quality of life and reduce compliance.79–81 Fifty percent to 70% of such medications are discontinued or changed within 6 months.82 Adherence to published guidelines for treatment of hypertension is poor, often with significant adverse impact on patients and the healthcare system.83,84 Other factors that may limit the effectiveness of medical therapy include temporal variations in drug levels and variable absorption.85,86 Finally, as described above, renal ischemia increases activity in a number of other pathogenic systems that may have deleterious cardiovascular or renal effects. Whether medical therapy alone is sufficient to minimize risk in patients with atherosclerotic RAS is not known.
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Intervention Cohort Studies |
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TopIntroductionRAS and HypertensionRAS and Kidney FunctionRAS and Cardiovascular EventsLimitations of Medical Therapy...Intervention Cohort StudiesLimitations of Nonrandomized...How Should Patients Be...ConclusionsReferences |
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An important feature of revascularization is the ability to obviate the root cause of the entire process: the stenotic renal artery. Importantly, others have demonstrated that relief of stenosis with revascularization results in a reduction in renin-angiotensin-aldosterone system and sympathetic activity.15 What is entirely unclear is whether pharmacological therapy directed at one or several of these pathways is equally effective or whether a reduction in activation attributable to revascularization leads to improvements in long-term clinical outcome.
In 1974, Hunt et al87 described lower rates of mortality, stroke, myocardial infarction, and azotemia and better blood pressure control in surgically revascularized patients than in a comparison medical group despite more severe hypertension in the revascularized subjects. Interestingly, in a more contemporary series comparing nonrandomized groups of patients with RAS and hypertension treated with stents or medications, Pizzolo et al88 reported a survival treatment effect in the intervention group similar to the experience of Hunt et al 30 years previously, with an 87% probability of 5-year survival in the intervention group versus 67% in the medical management group.
A number of single-center registries of stenting89 and a recent multicenter registry of stenting for failed balloon angioplasty90 suggest substantial benefits related primarily to improved blood pressure control. In contrast, the 3 multicenter trials of percutaneous balloon renal angioplasty (PTRA) without stenting failed to demonstrate a blood pressure benefit.91–93 Importantly, the randomized clinical trials done thus far have substantial weaknesses that have been the subject of considerable debate and discussion. The largest randomized trial comparing drug treatment and PTRA was the Dutch Renal Artery Stenosis Intervention Cooperative (DRASTIC) study. In this study, 106 patients were randomly assigned to treatment by PTRA or medical therapy. The study design was such that refractory patients in the drug therapy group were allowed to receive balloon angioplasty if their blood pressure control was inadequate. With 44% of the drug therapy group receiving PTRA, the study contrasted provisional angioplasty against angioplasty. Despite the authors’ assertion that PTRA in addition to drug therapy provided "little benefit," patients in the PTRA group were less likely to have deterioration of their blood pressure control or renal artery occlusion during 12 months of follow-up. Two other studies of balloon angioplasty versus medical therapy were confounded by similar issues and failed to demonstrate differences in blood pressure control.79,82 Importantly, none of the studies comparing PTRA and drug therapy thus far have included substantial numbers of patients who received stents.93 Renal artery stent placement is standard today and substantially improves technical and long-term clinical outcomes compared with angioplasty alone,89,94,95 especially for ostial stenoses,96 which make up 80% of atherosclerotic stenoses.97 In a meta-analysis of 1322 patients, stent placement had a higher technical success rate and a lower restenosis rate than did PTRA (98% versus 77% and 17% versus 26%, respectively; P<0.001) and a higher cure rate for hypertension.94
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Limitations of Nonrandomized Evidence |
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TopIntroductionRAS and HypertensionRAS and Kidney FunctionRAS and Cardiovascular EventsLimitations of Medical Therapy...Intervention Cohort StudiesLimitations of Nonrandomized...How Should Patients Be...ConclusionsReferences |
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There is little controversy that stenting is an effective means of achieving durable revascularization of the renal artery. Similarly, there is a wealth of uncontrolled study data demonstrating that some patients receive substantial benefits in blood pressure control and renal function.89,94,98,99 However, renal function worsens in some individuals after revascularization, and blood pressure may not improve. The current controversy is driven by a singular key factor: the lack of an appropriate control group to allow the magnitude of the benefit derived from stenting to be measured. Does stent revascularization markedly reduce the risk of cardiovascular and renal events, does it modestly reduce events, or are the risks of stenting balanced or even overwhelmed by complications? This determination has fundamental implications in the decisions that physicians make. If stenting has substantial benefits, then screening programs for high-, moderate-, or potentially even low-risk individuals become advisable. In contrast, if the benefit is small or marginal, then screening and treatment may be reserved for those at high risk. Furthermore, identifying subsets that derive greater or lesser benefit or even harm becomes possible when the relative benefits and risks can be identified.
Undoubtedly, some patients with atherosclerotic RAS appear to have a very favorable response to revascularization as determined by improvement in blood pressure or kidney function. Previous investigators have suggested that the response to revascularization may be predicted by the presence of microvascular dysfunction measured with the renal resistive index100 or by the presence of neurohumoral activation.55 Fundamentally, though, each of these observations is limited by the absence of a contrasting group of medically managed patients who are concurrent and carefully controlled. Thus, all such observations suggest but are unable to establish the relative benefit of revascularization or the true value of the baseline test strategy to predict outcome with differing treatments. This limitation, the absence of a robust and appropriate control group, has led to false conclusions, later disproved with appropriate randomized trials, about the utility of a wide variety of clinical therapies, including surgery for Ménière’s disease,101 warfarin for acute myocardial infarction,102 portosystemic shunts,103 and antiarrhythmic therapy after myocardial infarction.104
This is likely to be important for patients with renal artery hypertension. In fact, in the Scottish and Newcastle series,92 55 patients with renovascular hypertension were randomized to angioplasty or medical therapy after a run-in period of 4 weeks. It was noted that significant decreases in blood pressure occurred before the initiation of treatment. Thus, the effect of revascularization on blood pressure, observed in cohort studies, may be confounded by regression to the mean.
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How Should Patients Be Managed? |
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TopIntroductionRAS and HypertensionRAS and Kidney FunctionRAS and Cardiovascular EventsLimitations of Medical Therapy...Intervention Cohort StudiesLimitations of Nonrandomized...How Should Patients Be...ConclusionsReferences |
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These issues have pragmatic implications for the various physicians who care for patients with ischemic renal disease. Many in the interventional community feel compelled to revascularize renal stenoses, even when found incidentally. In 2000, an estimated 19 800 renal angioplasties were performed for Medicare beneficiaries alone at an estimated cost of $200 million.105 From 1996 to 2000, the annual number of renal stent procedures has increased 364%.105
In contrast, such enthusiasm is largely absent among nephrologists and others who routinely care for patients with chronic kidney diseases. Importantly, without widespread screening by the medical community, it is apparent that most patients with renovascular disease never come to attention. Recent work suggests that 
7% of individuals >65 years of age have significant RAS.106 Clearly, the majority are never identified within our communities, and far fewer are treated with either appropriate medical therapy or revascularization and medical therapy. This nihilistic approach of "no screen, no treat" may be proximate to the occurrence of a number of preventable cardiovascular and renal events.
Is there an exit to this conundrum? Yes. The National Heart, Lung, and Blood Institute has funded a pivotal trial, Cardiovascular Outcomes in Renal Atherosclerotic Lesions (CORAL), that is currently randomizing 1080 patients to optimal medical therapy versus optimal medical therapy with stenting, with a primary outcome consisting of a composite of attributable cardiovascular and renal events (www.coralclinicaltrial.org). At the present time, however, examining the published data provides little confidence that either intervention or medical management is superior for any given individual.
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Conclusions |
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TopIntroductionRAS and HypertensionRAS and Kidney FunctionRAS and Cardiovascular EventsLimitations of Medical Therapy...Intervention Cohort StudiesLimitations of Nonrandomized...How Should Patients Be...ConclusionsReferences |
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The case in favor of renal artery stenting is highly circumstantial but directionally consistent with important benefits of revascularization. Many of the physiological changes linked to adverse cardiovascular events may be improved with the durable relief of renal ischemia provided by stent therapy, including hypertension, sympathetic nervous system activation, oxidative stress, and direct hormone-mediated end-organ damage. In contrast, medication regimens may not be as effective, and their use may be limited by side effects that influence compliance. Nonrandomized comparisons suggest superior survival with revascularization compared with medical therapy.18,87 The published randomized trials that have compared blood-pressure lowering between patients who are treated medically and those treated with renal artery angioplasty have shown no benefit of balloon angioplasty, a therapy of largely historical interest for the treatment of atherosclerotic RAS. The current debate about the role of stent revascularization will undoubtedly continue until powerful and adequately controlled clinical trials are available that place the absolute and relative benefits of revascularization within the context of meaningful clinical events.
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Acknowledgments |
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Disclosures
Drs Cooper and Murphy are supported by NIH U01HL071556 and have grant funding from AstraZeneca, Pfizer, and Cordis corporations. Dr Cooper also has grant funding from Centocor Corp.
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References |
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TopIntroductionRAS and HypertensionRAS and Kidney FunctionRAS and Cardiovascular EventsLimitations of Medical Therapy...Intervention Cohort StudiesLimitations of Nonrandomized...How Should Patients Be...ConclusionsReferences |
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1. Goldblatt H, Lynch J, Hanzal RF, Summerville WW. Studies on experimental hypertension: production of persistent elevation of systolic blood pressure by means of renal ischemia. J Exp Med. 1934; 59: 347–379.Abstract.[Abstract]
2. Van Velzer DA, Burge CH, Morris GC Jr. Arteriosclerotic narrowing of renal arteries associated with hypertension. Am J Roentgenol Radium Ther Nucl Med. 1961; 86: 807–818.[Medline] [Order article via Infotrieve]
3. Lonn EM, Yusuf S, Jha P, Montague TJ, Teo KK, Benedict CR, Pitt B. Emerging role of angiotensin-converting enzyme inhibitors in cardiac and vascular protection. Circulation. 1994; 90: 2056–2069.
4. Meyrier A. Vascular mechanisms of renal fibrosis: vasculonephropathies and arterial hypertension. Bull Acad Natl Med. 1999; 183: 33–45.[Medline] [Order article via Infotrieve]
5. Vensel LA, Devereux RB, Pickering TG, Herrold EM, Borer JS, Laragh JH. Cardiac structure and function in renovascular hypertension produced by unilateral and bilateral renal artery stenosis. Am J Cardiol. 1986; 58: 575–582.[CrossRef][Medline] [Order article via Infotrieve]
6. Korner PI. Cardiovascular hypertrophy and hypertension: causes and consequences. Blood Press. 1995; 2: 6–16.[Medline] [Order article via Infotrieve]
7. Martin LG, Cork RD, Wells JO. Renal vein renin analysis: limitations of its use in predicting benefit from percutaneous angioplasty. Cardiovasc Intervent Radiol. 1993; 16: 76–80.[Medline] [Order article via Infotrieve]
8. Schreij G, van Es PN, Schiffers PM, Lavrijssen AT, de Leeuw PW. "Captopril test," with blood pressure and peripheral renin as response variables in hypertensive patients with suspected renal artery stenosis. J Hum Hypertens. 1995; 9: 741–746.[Medline] [Order article via Infotrieve]
9. Liard JF, Cowley AW Jr, McCaa RE, McCaa CS, Guyton AC. Renin, aldosterone, body fluid volumes, and the baroreceptor reflex in the development and reversal of Goldblatt hypertension in conscious dogs. Circ Res. 1974; 34: 549–560.
10. Ayers CR. Renin-angiotensin-aldosterone system in hypertension: the clinical usefulness of measuring components of this system. Va Med Mon (1918). 1969; 96: 312–314.[Medline] [Order article via Infotrieve]
11. Bianchi G, Campolo L, Vegeto A, Pietra V, Piazza U. The value of plasma renin concentration per se, and in relation to plasma and extracellular fluid volume in diagnosis and prognosis of human renovascular hypertension. Clin Sci. 1970; 39: 559–576.[Medline] [Order article via Infotrieve]
12. Anderson WP, Korner PI, Angus JA, Johnston CI. Contribution of stenosis resistance to the rise in total peripheral resistance during experimental renal hypertension in conscious dogs. Clin Sci (Lond). 1981; 61: 663–670.[Medline] [Order article via Infotrieve]
13. Schoenberg SO, Bock M, Kallinowski F, Just A. Correlation of hemodynamic impact and morphologic degree of renal artery stenosis in a canine model. J Am Soc Nephrol. 2000; 11: 2190–2198.
14. Johansson M, Elam M, Rundqvist B, Eisenhofer G, Herlitz H, Lambert G, Friberg P. Increased sympathetic nerve activity in renovascular hypertension. Circulation. 1999; 99: 2537–2542.
15. Miyajima E, Yamada Y, Yoshida Y, Matsukawa T, Shionoiri H, Tochikubo O, Ishii M. Muscle sympathetic nerve activity in renovascular hypertension and primary aldosteronism. Hypertension. 1991; 17: 1057–1062.
16. Mathias CJ, Kooner JS, Peart S. Neurogenic components of hypertension in human renal artery stenosis. Clin Exp Hypertens A. 1987; 9: 293–306.[CrossRef][Medline] [Order article via Infotrieve]
17. Higashi Y, Sasaki S, Nakagawa K, Matsuura H, Oshima T, Chayama K. Endothelial function and oxidative stress in renovascular hypertension. N Engl J Med. 2002; 346: 1954–1962.
18. Pizzolo F, Pavan C, Guarini P, Trabetti E, Girelli D, Corrocher R, Olivieri O. Primary hyperaldosteronism: a frequent cause of residual hypertension after successful endovascular treatment of renal artery disease. J Hypertens. 2005; 23: 2041–2047.[Medline] [Order article via Infotrieve]
19. Ye S, Ozgur B, Campese VM. Renal afferent impulses, the posterior hypothalamus, and hypertension in rats with chronic renal failure. Kidney Int. 1997; 51: 722–727.[Medline] [Order article via Infotrieve]
20. Converse RL Jr, Jacobsen TN, Jost CM, Toto RD, Grayburn PA, Obregon TM, Fouad-Tarazi F, Victor RG. Paradoxical withdrawal of reflex vasoconstriction as a cause of hemodialysis-induced hypotension. J Clin Invest. 1992; 90: 1657–1665.[Medline] [Order article via Infotrieve]
21. Chabova V, Schirger A, Stanson AW, McKusick MA, Textor SC. Outcomes of atherosclerotic renal artery stenosis managed without revascularization. Mayo Clin Proc. 2000; 75: 437–444.[Medline] [Order article via Infotrieve]
22. Wollenweber J, Sheps SG, Davis GD. Clinical course of atherosclerotic renovascular disease. Am J Cardiol. 1968; 21: 60–71.[CrossRef][Medline] [Order article via Infotrieve]
23. La Batide-Alanore A, Azizi M, Froissart M, Raynaud A, Plouin PF. Split renal function outcome after renal angioplasty in patients with unilateral renal artery stenosis. J Am Soc Nephrol. 2001; 12: 1235–1241.
24. Watson PS, Hadjipetrou P, Cox SV, Piemonte TC, Eisenhauer AC. Effect of renal artery stenting on renal function and size in patients with atherosclerotic renovascular disease. Circulation. 2000; 102: 1671–1677.
25. Harden PN, MacLeod MJ, Rodger RS, Baxter GM, Connell JM, Dominiczak AF, Junor BJ, Briggs JD, Moss JG. Effect of renal-artery stenting on progression of renovascular renal failure. Lancet. 1997; 349: 1133–1136.[CrossRef][Medline] [Order article via Infotrieve]
26. Dean RH, Kieffer RW, Smith BM, Oates JA, Nadeau JH, Hollifield JW, DuPont WD. Renovascular hypertension: anatomic and renal function changes during drug therapy. Arch Surg. 1981; 116: 1408–1415.
27. Meaney TF, Dustan HP, McCormack LJ. Natural history of renal arterial disease. Radiology. 1968; 91: 881–887.[Medline] [Order article via Infotrieve]
28. Tollefson DF, Ernst CB. Natural history of atherosclerotic renal artery stenosis associated with aortic disease. J Vasc Surg. 1991; 14: 327–331.[CrossRef][Medline] [Order article via Infotrieve]
29. Schreiber MJ, Pohl MA, Novick AC. The natural history of atherosclerotic and fibrous renal artery disease. Urol Clin North Am. 1984; 11: 383–392.[Medline] [Order article via Infotrieve]
30. Guzman RP, Zierler RE, Isaacson JA, Bergelin RO, Strandness DE Jr. Renal atrophy and arterial stenosis: a prospective study with duplex ultrasound. Hypertension. 1994; 23: 346–350.
31. Caps MT, Zierler RE, Polissar NL, Bergelin RO, Beach KW, Cantwell-Gab K, Casadei A, Davidson RC, Strandness DE Jr. Risk of atrophy in kidneys with atherosclerotic renal artery stenosis. Kidney Int. 1998; 53: 735–742.[CrossRef][Medline] [Order article via Infotrieve]
32. Zierler RE, Bergelin RO, Isaacson JA, Strandness DE Jr. Natural history of atherosclerotic renal artery stenosis: a prospective study with duplex ultrasonography. J Vasc Surg. 1994; 19: 250–257.[Medline] [Order article via Infotrieve]
33. Wright JR, Shurrab AE, Cheung C, Waldek S, O’Donoghue DJ, Foley RN, Mamtora H, Kalra PA. A prospective study of the determinants of renal functional outcome and mortality in atherosclerotic renovascular disease. Am J Kidney Dis. 2002; 39: 1153–1161.[CrossRef][Medline] [Order article via Infotrieve]
34. Suresh M, Laboi P, Mamtora H, Kalra PA. Relationship of renal dysfunction to proximal arterial disease severity in atherosclerotic renovascular disease. Nephrol Dial Transplant. 2000; 15: 631–636.
35. Morgan T, Wilson M, Johnston W, Clunie GJ, Gordon R. Restoration of renal function by arterial surgery. Lancet. 1974; 1: 653–656.[Medline] [Order article via Infotrieve]
36. Textor SC. Pathophysiology of renal failure in renovascular disease. Am J Kidney Dis. 1994; 24: 642–651.[Medline] [Order article via Infotrieve]
37. Volpe M, Camargo MJ, Mueller FB, Campbell WG Jr, Sealey JE, Pecker MS, Sosa RE, Laragh JH. Relation of plasma renin to end organ damage and to protection of K+ feeding in stroke-prone hypertensive rats. Hypertension. 1990; 15: 318–326.
38. Teunissen KE, Postma CT, van Jaarsveld BC, Derkx FH, Thien T. Endothelin and active renin levels in essential hypertension and hypertension with renal artery stenosis before and after percutaneous transluminal renal angioplasty. J Hypertens. 1997; 15: 1791–1796.[CrossRef][Medline] [Order article via Infotrieve]
39. Gobe GC, Axelsen RA, Searle JW. Cellular events in experimental unilateral ischemic renal atrophy and in regeneration after contralateral nephrectomy. Lab Invest. 1990; 63: 770–779.[Medline] [Order article via Infotrieve]
40. Sheps SG, Osmundson PJ, Hunt JC, Schirger A, Fairbairn JF 2nd. Hypertension and renal artery stenosis: serial observations on 54 patients treated medically. Clin Pharmacol Ther. 1965; 6: 700–709.[Medline] [Order article via Infotrieve]
41. Isles C, Main J, O’Connell J, Brown I, Findlay J, Stewart R, Wilkinson R. Survival associated with renovascular disease in Glasgow and Newcastle: a collaborative study. Scott Med J. 1990; 35: 70–73.[Medline] [Order article via Infotrieve]
42. Valentine RJ, Myers SI, Miller GL, Lopez MA, Clagett GP. Detection of unsuspected renal artery stenoses in patients with abdominal aortic aneurysms: refined indications for preoperative aortography. Ann Vasc Surg. 1993; 7: 220–224.[CrossRef][Medline] [Order article via Infotrieve]
43. Conlon PJ, Little MA, Pieper K, Mark DB. Severity of renal vascular disease predicts mortality in patients undergoing coronary angiography. Kidney Int. 2001; 60: 1490–1497.[CrossRef][Medline] [Order article via Infotrieve]
44. Losito A, Fagugli RM, Zampi I, Parente B, de Rango P, Giordano G, Cao P. Comparison of target organ damage in renovascular and essential hypertension. Am J Hypertens. 1996; 9: 1062–1067.[CrossRef][Medline] [Order article via Infotrieve]
45. de Simone G, Devereux RB, Volpe M, Camargo MJ, Wallerson DC, Laragh JH. Relation of left ventricular hypertrophy, afterload, and contractility to left ventricular performance in Goldblatt hypertension. Am J Hypertens. 1992; 5: 292–301.[Medline] [Order article via Infotrieve]
46. Gavras H, Lever AF, Brown JJ, Macadam RF, Robertson JI. Acute renal failure, tubular necrosis, and myocardial infarction induced in the rabbit by intravenous angiotensin II. Lancet. 1971; 2: 19–22.[CrossRef][Medline] [Order article via Infotrieve]
47. Yamazaki T, Shiojima I, Komuro I, Nagai R, Yazaki Y. Involvement of the renin-angiotensin system in the development of left ventricular hypertrophy and dysfunction. J Hypertens. 1994; 12: S153–S157.
48. Hocher B, George I, Rebstock J, Bauch A, Schwarz A, Neumayer HH, Bauer C. Endothelin system-dependent cardiac remodeling in renovascular hypertension. Hypertension. 1999; 33: 816–822.
49. Wahlander H, Isgaard J, Jennische E, Friberg P. Left ventricular insulin-like growth factor I increases in early renal hypertension. Hypertension. 1992; 19: 25–32.
50. Robertson AL Jr, Khairallah PA. Angiotensin II: rapid localization in nuclei of smooth and cardiac muscle. Science. 1971; 172: 1138–1139.
51. Ehmke H, Faulhaber J, Munter K, Kirchengast M, Wiesner RJ. Chronic ETA receptor blockade attenuates cardiac hypertrophy independently of blood pressure effects in renovascular hypertensive rats. Hypertension. 1999; 33: 954–960.
52. Phillips PA. Interaction between endothelin and angiotensin II. Clin Exp Pharmacol Physiol. 1999; 26: 517–518.[CrossRef][Medline] [Order article via Infotrieve]
53. Iwanaga Y, Kihara Y, Inagaki K, Onozawa Y, Yoneda T, Kataoka K, Sasayama S. Differential effects of angiotensin II versus endothelin-1 inhibitions in hypertrophic left ventricular myocardium during transition to heart failure. Circulation. 2001; 104: 606–612.
54. Pessina AC, Sacchetto A, Rossi GP. Left ventricular anatomy and function in primary aldosteronism and renovascular hypertension. Adv Exp Med Biol. 1997; 432: 63–69.[Medline] [Order article via Infotrieve]
55. Silva JA, Chan AW, White CJ, Collins TJ, Jenkins JS, Reilly JP, Ramee SR. Elevated brain natriuretic peptide predicts blood pressure response after stent revascularization in patients with renal artery stenosis. Circulation. 2005; 111: 328–333.
56. Broughton A, Korner PI. Left ventricular pump function in renal hypertensive dogs with cardiac hypertrophy. Am J Physiol. 1986; 251: H1260–H1266.[Medline] [Order article via Infotrieve]
57. Kannel WB. Role of blood pressure in cardiovascular disease: the Framingham study. Angiology. 1975; 26: 1–14.[Medline] [Order article via Infotrieve]
58. Meissner MD, Wilson AR, Jessup M. Renal artery stenosis in heart failure. Am J Cardiol. 1988; 62: 1307–1308.[CrossRef][Medline] [Order article via Infotrieve]
59. Olin JW. Atherosclerotic renovascular disease: diagnosis and management. Curr Opin Cardiol. 1990; 5: 659–665.[Medline] [Order article via Infotrieve]
60. Khosla S, White CJ, Collins TJ, Jenkins JS, Shaw D, Ramee SR. Effects of renal artery stent implantation in patients with renovascular hypertension presenting with unstable angina or congestive heart failure. Am J Cardiol. 1997; 80: 363–366.[CrossRef][Medline] [Order article via Infotrieve]
61. MacDowall P, Kalra PA, O’Donoghue DJ, Waldek S, Mamtora H, Brown K. Risk of morbidity from renovascular disease in elderly patients with congestive cardiac failure. Lancet. 1998; 352: 13–16.[CrossRef][Medline] [Order article via Infotrieve]
62. MacMahon S, Peto R, Cutler J, Collins R, Sorlie P, Neaton J, Abbott R, Godwin J, Dyer A, Stamler J. Blood pressure, stroke, and coronary heart disease, part 1: prolonged differences in blood pressure: prospective observational studies corrected for the regression dilution bias. Lancet. 1990; 335: 765–774.[CrossRef][Medline] [Order article via Infotrieve]
63. Sorensen MB, Bille Brahe NE. Preoperative haemodynamic evaluation of patients submitted for renal artery stenosis. Acta Anaesthesiol Scand. 1984; 28: 334–338.[Medline] [Order article via Infotrieve]
64. MacMahon S, Collins G, Rautaharju P, Cutler J, Neaton J, Prineas R, Crow R, Stamler J. Electrocardiographic left ventricular hypertrophy and effects of antihypertensive drug therapy in hypertensive participants in the Multiple Risk Factor Intervention Trial. Am J Cardiol. 1989; 63: 202–210.[CrossRef][Medline] [Order article via Infotrieve]
65. Culleton BF, Larson MG, Wilson PW, Evans JC, Parfrey PS, Levy D. Cardiovascular disease and mortality in a community-based cohort with mild renal insufficiency. Kidney Int. 1999; 56: 2214–2219.[CrossRef][Medline] [Order article via Infotrieve]
66. Levy D, Garrison RJ, Savage DD, Kannel WB, Castelli WP. Prognostic implications of echocardiographically determined left ventricular mass in the Framingham Heart Study. N Engl J Med. 1990; 322: 1561–1566.[Abstract]
67. Kannel WB. Left ventricular hypertrophy as a risk factor: the Framingham experience. J Hypertens Suppl. 1991; 9: S3–S8.[Medline] [Order article via Infotrieve]
68. Kannel WB, Cobb J. Left ventricular hypertrophy and mortality: results from the Framingham study. Cardiology. 1992; 81: 291–298.[Medline] [Order article via Infotrieve]
69. Devereux RB, Okin PM, Roman MJ. Left ventricular hypertrophy as a surrogate end-point in hypertension. Clin Exp Hypertens. 1999; 21: 583–593.[CrossRef][Medline] [Order article via Infotrieve]
70. Sullivan JM, Vander Zwaag RV, el-Zeky F, Ramanathan KB, Mirvis DM. Left ventricular hypertrophy: effect on survival. J Am Coll Cardiol. 1993; 22: 508–513.[Abstract]
71. Brown MJ, Castaigne A, de Leeuw PW, Mancia G, Palmer CR, Rosenthal T, Ruilope LM. Influence of diabetes and type of hypertension on response to antihypertensive treatment. Hypertension. 2000; 35: 1038–1042.
72. Symonides B, Chodakowska J, Januszewicz A, Lapinski M, Januszewicz M, Rowinski O, Szmidt J, Kuch-Wocial A, Kurzyna M, Malek G, Berent H, Szmigielski C, Januszewicz W. Effects of the correction of renal artery stenosis on blood pressure, renal function and left ventricular morphology. Blood Press. 1999; 8: 141–150.[CrossRef][Medline] [Order article via Infotrieve]
73. Missouris CG, Belli AM, MacGregor GA. "Apparent" heart failure: a syndrome caused by renal artery stenoses. Heart. 2000; 83: 152–155.
74. Hirsch AT, Haskal ZJ, Hertzer NR, Bakal CW, Creager MA, Halperin JL, Hiratzka LF, Murphy WR, Olin JW, Puschett JB, Rosenfield KA, Sacks D, Stanley JC, Taylor LM Jr, White CJ, White J, White RA, Antman EM, Smith SC Jr, Adams CD, Anderson JL, Faxon DP, Fuster V, Gibbons RJ, Hunt SA, Jacobs AK, Nishimura R, Ornato JP, Page RL, Riegel B. ACC/AHA 2005 practice guidelines for the management of patients with peripheral arterial disease. Circulation. 2006; 113: e463–e654.
75. Brenner BM, Cooper ME, de Zeeuw D, Keane WF, Mitch WE, Parving HH, Remuzzi G, Snapinn SM, Zhang Z, Shahinfar S. Effects of losartan on renal and cardiovascular outcomes in patients with type 2 diabetes and nephropathy. N Engl J Med. 2001; 345: 861–869.
76. Lewis EJ, Hunsicker LG, Clarke WR, Berl T, Pohl MA, Lewis JB, Ritz E, Atkins RC, Rohde R, Raz I. Renoprotective effect of the angiotensin-receptor antagonist irbesartan in patients with nephropathy due to type 2 diabetes. N Engl J Med. 2001; 345: 851–860.
77. Dagenais GR, Yusuf S, Bourassa MG, Yi Q, Bosch J, Lonn EM, Kouz S, Grover J. Effects of ramipril on coronary events in high-risk persons: results of the Heart Outcomes Prevention Evaluation Study. Circulation. 2001; 104: 522–526.
78. Dahlof B, Zanchetti A, Diez J, Nicholls MG, Yu CM, Barrios V, Aurup P, Smith RD, Johansson M. Effects of losartan and atenolol on left ventricular mass and neurohormonal profile in patients with essential hypertension and left ventricular hypertrophy. J Hypertens. 2002; 20: 1855–1864.[CrossRef][Medline] [Order article via Infotrieve]
79. Curb JD, Borhani NO, Blaszkowski TP, Zimbaldi N, Fotiu S, Williams W. Long-term surveillance for adverse effects of antihypertensive drugs. JAMA. 1985; 253: 3263–3268.
80. MRC trial of treatment of mild hypertension: principal results: Medical Research Council Working Party. BMJ (Clin Res Ed). 1985; 291: 97–104.
81. Stewart AL, Greenfield S, Hays RD, Wells K, Rogers WH, Berry SD, McGlynn EA, Ware JE Jr. Functional status and well-being of patients with chronic conditions: results from the Medical Outcomes Study. JAMA. 1989; 262: 907–913.
82. Oparil S, Calhoun DA. The calcium antagonists in the 1990s: an overview. Am J Hypertens. 1991; 4: 396S–405S.[Medline] [Order article via Infotrieve]
83. Siegel D, Lopez J, Meier J, Cunningham F. Changes in the pharmacologic treatment of hypertension in the Department of Veterans Affairs 1997–1999: decreased use of calcium antagonists and increased use of beta-blockers and thiazide diuretics. Am J Hypertens. 2001; 14: 957–962.[CrossRef][Medline] [Order article via Infotrieve]
84. Okano GJ, Rascati KL, Wilson JP, Remund DD. A comparison of antihypertensive medication utilization before and after guideline changes using the Department of Defense Prescription Database. Ann Pharmacother. 1999; 33: 548–553.[Abstract]
85. Campbell DJ. Endogenous angiotensin II levels and the mechanism of action of angiotensin-converting enzyme inhibitors and angiotensin receptor type 1 antagonists. Clin Exp Pharmacol Physiol. 1996; 3: S125–S131.
86. Wolny A, Clozel JP, Rein J, Mory P, Vogt P, Turino M, Kiowski W, Fischli W. Functional and biochemical analysis of angiotensin II-forming pathways in the human heart. Circ Res. 1997; 80: 219–227.
87. Hunt JC, Sheps SG, Harrison EG Jr, Strong CG, Bernatz PE. Renal and renovascular hypertension: a reasoned approach to diagnosis and management. Arch Intern Med. 1974; 133: 988–999.
88. Blum U, Krumme B, Flugel P, Gabelmann A, Lehnert T, Buitrago-Tellez C, Schollmeyer P, Langer M. Treatment of ostial renal-artery stenoses with vascular endoprostheses after unsuccessful balloon angioplasty. N Engl J Med. 1997; 336: 459–465.
89. Pizzolo F, Mansueto G, Minniti S, Mazzi M, Trabetti E, Girelli D, Corrocher R, Olivieri O. Renovascular disease: effect of ACE gene deletion polymorphism and endovascular revascularization. J Vasc Surg. 2004; 39: 140–147.[CrossRef][Medline] [Order article via Infotrieve]
90. Rees CR, Palmaz JC, Becker GJ, Ehrman KO, Richter GM, Noeldge G, Katzen BT, Dake MD, Schwarten DE. Palmaz stent in atherosclerotic stenoses involving the ostia of the renal arteries: preliminary report of a multicenter study. Radiology. 1991; 181: 507–514.
91. Plouin PF, Chatellier G, Darne B, Raynaud A. Blood pressure outcome of angioplasty in atherosclerotic renal artery stenosis: a randomized trial: Essai Multicentrique Medicaments vs Angioplastie (EMMA) Study Group. Hypertension. 1998; 31: 823–829.
92. Webster J, Marshall F, Abdalla M, Dominiczak A, Edwards R, Isles CG, Loose H, Main J, Padfield P, Russell IT, Walker B, Watson M, Wilkinson R. Randomised comparison of percutaneous angioplasty vs continued medical therapy for hypertensive patients with atheromatous renal artery stenosis: Scottish and Newcastle Renal Artery Stenosis Collaborative Group. J Hum Hypertens. 1998; 12: 329–335.[CrossRef][Medline] [Order article via Infotrieve]
93. van Jaarsveld BC, Krijnen P, Pieterman H, Derkx FH, Deinum J, Postma CT, Dees A, Woittiez AJ, Bartelink AK, Man in ’t Veld AJ, Schalekamp MA. The effect of balloon angioplasty on hypertension in atherosclerotic renal-artery stenosis: Dutch Renal Artery Stenosis Intervention Cooperative Study Group. N Engl J Med. 2000; 342: 1007–1014.
94. Leertouwer TC, Gussenhoven EJ, Bosch JL, van Jaarsveld BC, van Dijk LC, Deinum J, Man In ’t Veld AJ. Stent placement for renal arterial stenosis: where do we stand? A meta-analysis. Radiology. 2000; 216: 78–85.
95. Hennequin LM, Joffre FG, Rousseau HP, Aziza R, Tregant P, Bernadet P, Salvador M, Chamontin B. Renal artery stent placement: long-term results with the Wallstent endoprosthesis. Radiology. 1994; 191: 713–719.
96. Baumgartner I, von Aesch K, Do DD, Triller J, Birrer M, Mahler F. Stent placement in ostial and nonostial atherosclerotic renal arterial stenoses: a prospective follow-up study. Radiology. 2000; 216: 498–505.
97. Kaatee R, Beek FJ, Verschuyl EJ, vd Ven PJ, Beutler JJ, van Schaik JP, Mali WP. Atherosclerotic renal artery stenosis: ostial or truncal? Radiology. 1996; 199: 637–640.
98. Burket MW, Cooper CJ, Kennedy DJ, Brewster PS, Ansel GM, Moore JA, Venkatesan J, Henrich WL. Renal artery angioplasty and stent placement: predictors of a favorable outcome. Am Heart J. 2000; 139: 64–71.[Medline] [Order article via Infotrieve]
99. Harding MB, Smith LR, Himmelstein SI, Harrison K, Phillips HR, Schwab SJ, Hermiller JB, Davidson CJ, Bashore TM. Renal artery stenosis: prevalence and associated risk factors in patients undergoing routine cardiac catheterization. J Am Soc Nephrol. 1992; 2: 1608–1616.[Abstract]
100. Radermacher J, Chavan A, Bleck J, Vitzthum A, Stoess B, Gebel MJ, Galanski M, Koch KM, Haller H. Use of Doppler ultrasonography to predict the outcome of therapy for renal-artery stenosis. N Engl J Med. 2001; 344: 410–417.
101. Snow JB Jr, Kimmelman CP. Assessment of surgical procedures for Meniere’s disease. Laryngoscope. 1979; 89: 737–747.[Medline] [Order article via Infotrieve]
102. Chalmers TC, Matta RJ, Smith H Jr, Kunzler AM. Evidence favoring the use of anticoagulants in the hospital phase of acute myocardial infarction. N Engl J Med. 1977; 297: 1091–1096.[Abstract]
103. Grace ND, Muench H, Chalmers TC. The present status of shunts for portal hypertension in cirrhosis. Gastroenterology. 1966; 50: 684–691.[Medline] [Order article via Infotrieve]
104. Preliminary report: effect of encainide and flecainide on mortality in a randomized trial of arrhythmia suppression after myocardial infarction: the Cardiac Arrhythmia Suppression Trial (CAST) Investigators. N Engl J Med. 1989; 321: 406–412.[Abstract]
105. Murphy TP, Soares G, Kim M. Increase in utilization of percutaneous renal artery interventions by Medicare beneficiaries, 1996–2000. AJR Am J Roentgenol. 2004; 183: 561–568.
106. Hansen KJ, Edwards MS, Craven TE, Cherr GS, Jackson SA, Appel RG, Burke GL, Dean RH. Prevalence of renovascular disease in the elderly: a population-based study. J Vasc Surg. 2002; 36: 443–451.[CrossRef][Medline] [Order article via Infotrieve]
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The opinions expressed in this article are not necessarily those of the editors or of the American Heart Association.
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