Abstract: Background. Concomitant renal artery stenosis (RAS) aggravates the presentations and outcomes of coronary artery disease. To date, no reports have been published on the feasibility, safety, and outcomes of concomitant percutaneous renal artery stenting (PTRS) in patients presenting with acute coronary syndrome (ACS) at high clinical risk of RAS. Methods. This was a retrospective study. Eighty-two patients who were at high clinical risk of RAS, undergoing simultaneous coronary and renal angiographies between January 2005 and July 2011, were queried from the data of 2186 ACS patients. Results. A total of 80 patients (48 males; age, 77 ± 8 years) were enrolled. Thirty-five patients (43.8%) were found to have significant RAS and all received PTRS. Peripheral arterial disease (PAD) was found to be the only predictive factor for RAS in multivariate analysis. There were no significant differences in the total procedural/fluoroscopic times or the volume of contrast used between RAS/PTRS and non-RAS groups. No extra procedure-related morbidities occurred in the RAS/PTRS group. There were no significant differences in serum creatinine, estimated glomerular filtration rate, or clinical outcomes between the groups at different follow-up points. However, the mean number of antihypertensives decreased significantly 3 months after PTRS. The systolic and diastolic blood pressures also significantly lowered 6 months after PTRS. Conclusions. Significant RAS was not infrequently found in ACS patients at high clinical risk. PAD was the only independent predictive factor. Concomitant PTRS could be safely and effectively performed in the same session as coronary interventions with favorable outcomes.
J INVASIVE CARDIOL 2013;25(5):212-217
Key words: acute coronary syndrome, renal artery stenosis, percutaneous transluminal renal artery stenting, peripheral arterial occlusive disease
Renal artery stenosis (RAS) is associated with increased cardiovascular morbidity and mortality. The association between RAS and systemic atherosclerosis is well known and patients with ischemic heart and peripheral arterial occlusive diseases (PAD) are at high risk (24%-27%) of RAS.1-4 Concomitant significant RAS (≥50%-70% diameter stenosis) also aggravates the clinical course of coronary artery disease (CAD). Despite coronary revascularization, survival in patients with both CAD and RAS is significantly lower.5,6 Recently, screening for RAS has gained more attention in CAD patients undergoing coronary angiography since early renal intervention may be associated with better control of hypertension, preservation of renal function, and improved outcomes in patients with CAD.7-9 However, diagnosis of RAS is difficult because its course can be clinically silent until end-stage renal failure, refractory hypertension, congestive heart failure (CHF), flash pulmonary edema, and/or acute coronary syndrome (ACS) occur. Furthermore, percutaneous renal artery stenting (PTRS) may cause significant complications.10,11 To date, no reports have been published on the feasibility, safety, and clinical outcomes of concomitant PTRS in patients presenting with ACS who are found to have significant RAS (≥70% diameter stenosis). The aim of the present study was to address this issue.
This study had a retrospective design. A Windows 2000-based cardiac catheterization report databank with Access 2000 software that uses the hospital information system data stored in the mainframe computer and contains the entire angiographic report data over the past 19 years has been installed in our cath lab. Between January 2005 and July 2011, the data on patients who were diagnosed as having ACS (unstable angina, ST- and non-ST elevation myocardial infarction) and underwent coronary and renal angiographies in the same session at our cath lab were retrospectively queried from the databank. Patients who underwent both angiographies on an elective basis or patients whose renal arteries could not be engaged were excluded. In our cath lab, simultaneous renal angiography during coronary angiographic study for ACS was restricted to patients if one or more of the following was/were present, making them at high clinical risk of RAS: renal insufficiency of undetermined cause, presence of advanced systemic arterial diseases, blood pressure higher than 140/90 mm Hg despite use of ≥4 kinds of antihypertensives, or flash pulmonary edema or recurrent CHF of undetermined cause. Renal insufficiency that could be ascribed to renal or postrenal origins documented in current or previous laboratory studies was not an indication for renal angiography. CHF that could be reasonably accounted for by severely depressed left ventricular function (ejection fraction ≤30%) or severe CAD was also not an indication for renal artery study. Advanced systemic arterial diseases were clinically suspected or diagnosed if there was prominent neck bruit, loss or decreased brachial, femoral, popliteal or leg pulses, or previous angiographic or ultrasonic documentations of significant lesions in the iliac, femoral, popliteal, or below-knee arteries.
During the study period, a total of 2186 patients underwent coronary angiography for ACS at our cath lab. Of these patients, eighty-two (3.8%) received simultaneous renal angiography due to high risk for significant RAS and were recruited. Two patients were excluded because their left renal arteries could not be engaged; hence, a total of 80 patients were enrolled in the study.
Angiographies and interventions. For patients who were going to have simultaneous renal and coronary angiographies, the procedures were performed via the femoral approach by operators experienced in both coronary and renal interventions, using standard Judkins technique. Following the diagnostic coronary angiography, the diagnostic Judkins Right catheter was pulled back to the L1/L2 level and manipulated to engage the renal arteries for selective angiography. If percutaneous coronary intervention (PCI) was indicated, it was performed for significant or culprit lesions by standard practice. PTRS was done in the same session following completion of PCI, also by standard practice as indicated in our previous report.12
The complete coronary and renal angiograms were reviewed independently by two cardiologists experienced in both coronary and renal artery interventions and blinded to patient’s clinical information. Coronary and renal angiographic measurements were made on a dedicated workstation with software for quantitative analysis of angiograms (Philips Inturis Suite R2.2; Philips Medical Systems). Significant CAD was defined as more than 50% reduction in diameter of at least one major epicardial artery and target lesion for revascularization needed to have ≥70% diameter stenosis. The extent of CAD severity was categorized as single-, double-, or triple-vessel disease. Significant RAS was defined as the presence of ≥50% luminal stenosis in one or both renal arteries and only lesions ≥70% diameter stenosis were treated. Ostial lesions were defined as stenoses located within 5 mm of the aortic lumen, proximal lesions 5-10 mm from the aortic lumen, and isolated truncal lesions more than 10 mm distally from the aortic lumen.13,14
Patient characteristics including age, gender, type of ACS, CAD severity, and atherosclerotic risk factors were retrospectively collected and recorded. Patient clinical information at admission was reviewed in detail through the medical chart and cath report and recorded, including presence of cardiogenic shock, acute pulmonary edema, respiratory failure demanding mechanical ventilation, and use of inotropes.
Hypertension was defined as either systolic blood pressure greater than 140 mm Hg, diastolic blood pressure greater than 90 mm Hg, or a previous diagnosis in patients currently taking antihypertensive medications. Dyslipidemia was defined as either a blood lipid profile fitting the diagnostic criteria (cholesterol level >240 mg/dL, triglyceride level >200 mg/dL, high-density lipoprotein level <40 mg/dL in men and <50 mg/dL in women, or low-density lipoprotein level > 160 mg/dL), or previous diagnosis in patients taking lipid-lowering drugs. PAD was defined as loss or diminishment of peripheral pulse amplitude by one or more grades from normal on palpation, or a previous diagnosis by angiographic or ultrasonic studies in the iliac, femoral, popliteal, or below-knee arteries with or without intervention.
Clinical follow-up and PTRS outcomes. Renal function was noted at baseline and at 3-7 days, 3 months, and 6 months postintervention; systemic blood pressure was noted at baseline, and at 3 and 6 months postintervention; and the number of antihypertensives used at baseline and at 3 months was obtained. Renal function was represented as serum creatinine and estimated glomerular filtration rate (eGFR). Improvement and deterioration in renal function were defined as a decrease and increase in serum creatinine of 20% or more, respectively. Data on all-cause death, procedure-related death, stroke, bleeding, contrast-induced nephropathy (CIN; transient deterioration of serum creatinine level of more than 15%), and unexpected dialysis within 30 days after intervention were collected and analyzed.
Statistical analysis. Continuous variables were presented as mean ± standard deviation (SD) and categorical variables were presented as frequencies and percentages. Differences in means of parameters between and within groups were tested by independent and paired t-tests, respectively. Differences in frequencies were analyzed with the Chi-square test. Univariate and stepwise multivariate logistic regression analyses were performed to identify clinical and angiographic variables predictive of significant RAS. SPSS 14.0 statistical software package (SPSS, Inc) was used for all calculations. Differences were considered significant if the P-value was <.05.
Patient characteristics. RAS was found in 35 of the 82 patients (43.8%) and all 35 RAS patients received PTRS. The clinical characteristics of the patients with and without RAS are summarized in Table 1. As a group, most of these patients presented with unstable angina (48/80; 60%) or NSTEMI (29/80; 36.3%). Acute pulmonary edema was present in 52/80 (62.5%) and endotracheal intubation was needed in 19/80 patients (23.8%). The mean serum creatinine was 2.6 ± 1.2 mg/dL. There were no significant differences in sex, age, hypertension, diabetes mellitus, smoking, or hyperlipidemia between the RAS/PTRS and the non-RAS groups, but the RAS/PTRS group had more PAD (51.4% vs 9.1%; P<.001). Though the RAS/PTRS group tended to have a higher serum creatinine level, the difference did not reach statistical significance (2.8 ± 1.4 mg/dL vs 2.4 ± 1.0 mg/dL; P=.160).
Clinical predictors of RAS. In univariate analysis, only PAD was significantly associated with presence of significant RAS (odds ratio [OR], 10.59; 95% confidence interval [CI], 3.12-35.97; P<.001), which could not be predicted by age, sex, hypertension, history of CAD, multiple vessel coronary disease, diabetes mellitus, hyperlipidemia, smoking, multiple antihypertensive medications, serum creatinine, systemic blood pressure, or presence of pulmonary edema. Using a stepwise multivariate logistic regression model, we found that PAD remained the only strong predictor for RAS in these patients (OR, 17.94; 95% CI, 3.22-100.11; P<.001).
Characteristics of coronary/renal angiographies and PTRS. The characteristics of coronary/renal angiographies and intervention details are summarized in Tables 1 and 2. Among these ACS patients, 7 (8.8%) had no significant coronary lesions, but significant RAS was present in 6 (85.7%). The non-RAS group had more right coronary artery lesions than the RAS/PTRS group (22 lesions vs 9; P<.035), but there were no differences in the numbers of left main, left anterior descending, or circumflex lesions.
In the RAS/PTRS group, the mean RAS was 87 ± 9% and most lesions were located in the ostium or the proximal segment of the renal arteries (30/42 [71.4%] and 9/42 [21.4%], respectively). Seven (20%) of RAS patients had bilateral renal artery lesions and a total of 40 renal stents were implanted. Two lesions were not treated because they were chronically totally occluded and had no identifiable distal blood flow. A distal protection device was utilized in 7 of these patients (20%) and at the discretion of the operators. The baseline serum creatinine was similar between patients who received PTRS with and without distal protection devices. There was no statistically significant difference in the volume of contrast medium used between the RAS/PTRS and the non-RAS groups. There were no significant differences in total procedural or fluoroscopic times between these two groups. No extra procedure-related complications occurred in patients who received PTRS.
Clinical and renal outcomes in the follow-up periods. The clinical and renal outcomes are presented in Table 3. There was no significant difference in serum creatinine or eGFR between the RAS/PTRS and non-RAS groups at the baseline or different follow-up time points. There was no significant difference in absolute changes in serum creatinine or eGFR at 6 months between these two groups. The within-individual changes in renal function in patients who underwent PTRS with distal protection devices were not different from those without. There was also no significant difference in the trichotomized (improved, stabilized, or deteriorated) renal outcomes at either 3-month or 6-month follow-up between the RAS/PTRS and the non-RAS groups.
The systolic and diastolic blood pressures were similar in the RAS/PTRS and non-RAS groups at baseline and at different follow-up time points. However, in the RAS/PTRS group, the systolic blood pressure was significantly lowered at the 3- and 6-month follow-up exams (both P<.001). The diastolic blood pressure was significantly lowered at 6-month follow-up (P=.049), but not at 3-month follow-up (P=.241). In the non-RAS group, systolic blood pressure was significantly lowered at 6-month follow-up (P=.029), but not at 3-month follow-up (P=.055). The diastolic blood pressure did not change significantly at either the 3-month or 6-month follow-up (P=.443 and .613, respectively). The mean number of antihypertensives used at 3 months after PTRS significantly decreased in the RAS/PTRS group (2.1 ± 0.8 vs 2.4 ± 0.9; P=.008), but the corresponding number increased significantly (2.4 ± 1.0 vs 2.1 ± 1.0; P<.001) in the non-RAS group (Figure 1).
There was a trend toward less CIN in the RAS/PTRS group compared to the non-RAS group (6/35 [17.1%] vs 15/45 [33.3%]; P=.059). Regarding clinical outcomes, there were 2 deaths (5.7%) within 30 days in the RAS/PTRS group, but neither of these was related to the given procedure. Four patients (11.4%) in the RAS/PTRS group and 1 patient in the non-RAS group (2.2%; P=.222) became dialysis-dependent during the follow-up.
In this study, we found that: (1) the presence of significant RAS was as high as 43.8% in ACS patients at high clinical risk of RAS who underwent simultaneous coronary and renal angiographies, and the incidence of bilateral renal arterial involvement was also high (20%) in those affected; (2) the presence of significant RAS could be predicted by the presence of PAD, but not by other factors; (3) non-coronary ACS was the sole presentation of RAS in 6/80 patients (7.5%) at high risk for RAS; and (4) significant RAS in association with ACS could be safely and effectively treated percutaneously in the same session as PCI with favorable clinical outcomes.
RAS has a high prevalence in risk groups, especially in those with extrarenal atherosclerosis, end-stage renal failure, and CHF.3 Previous studies found a prevalence rate of 5.4%-30% of RAS in patients undergoing cardiac catheterization.1,2,15-17 The reported prevalence rate of RAS was 16.6% (14.8%-18.5%) and 17.8% (15.4%-20.6%) in coronary angiographic (CAG) patients with suspected renovascular disease and with hypertension, respectively. The prevalence of RAS was as high as 23.6%-27% in patients with PAD and up to 54.1% in CHF patients.3 However, the prevalence of RAS in ACS patients at high risk of significant RAS has not been reported. The prevalence rate was 43.8% in the present study, again confirming the importance of RAS in these high-risk patients. Furthermore, 20% of our patients with RAS presented bilateral renal arterial involvements, a percentage that was higher than reported in previous studies,1,4,15 and arguing for the advanced atherosclerosis in these high-risk patients. Progression in atheromatous plaques leads to the aggravation of RAS and PAD. Therefore, it is not surprising that in our study RAS was predicted by PAD alone in multivariate analysis. Our findings emphasized the importance of identifying PAD by physical exam or lab studies in morbid ACS patients in order to find potential significant RAS so that both angiographic diagnosis and interventional treatment of RAS can be part of the ad hoc treatment plan.
Significant RAS usually presents as high blood pressure, renal insufficiency, acute pulmonary edema, or acute CHF.6,18,19 Of patients with incidentally found RAS, hypertension and renal failure were present in 65.5% and 27.5%, respectively.3 The mechanism of hypertension and cardiac morbidities in RAS is complex, often not strictly renin-dependent but with an interplay between vasculotoxic effects of renin, proinflammatory, and neurohormonal effects of angiotensin and endocrinological effects of aldosterone.20 In the present study, we found that a small portion of ACS-presenting cases were caused by significant RAS per se, but not coronary lesions. This should remind us that renal angiographic study needs to be especially considered in those patients in whom coronary lesions do not fully account for their ACS disease severity.
Renal artery disease progression was found in 11.1% of patients with RAS and there was a significant elevation in serum creatinine during a 2.6 ± 1.6 year follow-up.18 Subsequent renal atrophy was also found in a significant proportion of RAS patients.21 The presence of RAS was associated with progression in extrarenal diseases like new-onset CAD, PAD, stroke, or CHF,11,22 and these occurred at around 10% per year follow-up in the ASTRAL study.11,22 Patients with RAS also have a high mortality rate. In the older Medicare cohort, the annual mortality rate was 16.3% and 8% in the ASTRAL study.11 Theoretically, treatment of the underlying RAS might halt the progression of renal disease and prevent adverse clinical outcomes. PTRS is widely used to treat atherosclerotic RAS.23 However, a recent meta-analysis failed to find a significant postintervention improvement in blood pressure or renal function in these patients,24 although the authors did find a trend toward benefit of renal revascularization plus medical therapy on blood pressure control (P=.07 for systolic blood pressure, P=.12 for diastolic blood pressure) and renal function (P=.07 for serum creatinine). However, these randomized studies used in meta-analysis were flawed by several limitations,24 including issues of patient selection, interventional skills, and devices used. Therefore, the reported results may not be generalizable to patients with critical RAS, RAS with strong clinical presentation, or ACS. Traditionally, percutaneous renal revascularization has been associated with some 10%-20% of worsening renal function or blood pressure after the procedure.11,25,26 The risks could even be higher in patients with severe background renal insufficiency26-28 and the causes could be multifactorial.28-30 There are several ways to improve renal revascularization, including routine stenting,31 delicacy in manipulation,12 reduction in contrast medium use, and application of distal protection.32,33 In the current study, improvement in renal function was found in 28% and 21% of patients at 3 and 6 months post PTRS, respectively, whereas deterioration of renal function was found in 19% at 3 months and 24% at 6 months. These percentages, which were similar to those reported in the literature,26-29 and in those patients not undergoing additional renal intervention (non-RAS group in the present study), were considered quite good given that these patients had severe underlying renal insufficiency and completed PCI before additional renal interventions were done. In our experience, the additional renal revascularization was performed without extra procedure-related complications, contrast medium volume, or procedural or fluoroscopic times. The fact that both the coronary and renal interventions in our study were done by operators experienced in both intervention fields might partially explain the PTRS results and low complication rate. However, the lack of differences in contrast volume or times could be attributable to small patient numbers, variations in PCI complexities prior to PTRS, or the fact that 6 patients in the RAS/PTRS received PTRS but no PCI.
In accordance with previous studies,34,35 our study also showed that the number of antihypertensives could be significantly reduced from baseline to 6 months, illustrating one benefit of PTRS in these patients. In contrast to previous studies,24,34 our study showed that the systemic blood pressure was significantly lowered 6 months after PTRS, demonstrating an additional benefit of PTRS in ACS patients with concomitant RAS. Moreover, our study showed a trend toward less CIN in the RAS/PTRS group as compared to the non-RAS group. In our study, distal protection devices were used in only 20% of patients, mostly because PTRS was done following PCI (which already took up some time) and our insurance system did not reimburse for distal protection devices. Though the use of distal protection devices did not affect the study results, the present study did not address this issue.
Study limitations. There are several limitations in our study. First of all, this was a retrospective, nonrandomized study, and as such was subject to all the inherent limitations therein. Second, although we accessed the medical data of 2186 ACS-diagnosed patients who had undergone interventional therapies during the 5-year study period, only a small number (3.8%) of these patients underwent simultaneous coronary and renal angiographies. Therefore, selection bias could not be avoided. However, the aim of our study was to investigate the prevalence of significant RAS and the feasibility, safety, and outcomes of concomitant PTRS only in ACS patients at high risk of RAS. The correct diagnosis and proper percutaneous treatment of the concomitant RAS had relevant clinical implications. Our study results might be provocative and further larger-scale prospective studies might shed more light on this issue.
Our study demonstrated that significant RAS was not infrequently found in ACS patients at high clinical risk of RAS, in whom the presence of PAD was the only independent predictive factor. These patients should be prepared for both coronary and renal studies and interventions if they are going to have invasive procedures. Some ACS cases were solely caused by significant renal lesions. Significant RAS in association with ACS could be safely and effectively treated percutaneously in the same session as PCI with favorable clinical results by operators experienced in both fields.
- Harding MB, Smith LR, Himmelstein SI, et al. Renal artery stenosis: prevalence and associated risk factors in patients undergoing routine cardiac catheterization. J Am Soc Nephrol. 1992;2(11):1608-1616.
- Buller CE, Nogareda JG, Ramanathan K, et al. The profile of cardiac patients with renal artery stenosis. J Am Coll Cardiol. 2004;43(9):1606-1613.
- de Mast Q, Beutler JJ. The prevalence of atherosclerotic renal artery stenosis in risk groups: a systematic literature review. J Hypertens. 2009;27(7):1333-1340.
- Carmelita M, Stefania R, Luca Z, et al. Prevalence of renal artery stenosis in patients undergoing cardiac catheterization. Intern Emerg Med. 2011 May 25 (Epub ahead of print).
- Conlon PJ, Athirakul K, Kovalik E, et al. Survival in renal vascular disease. J Am Soc Nephrol. 1998;9(2):252-256.
- Conlon PJ, Little MA, Pieper K, Mark DB. Severity of renal vascular disease predicts mortality in patients undergoing coronary angiography. Kidney Int. 2001;60(4):1490-1497.
- White CJ. Catheter-based therapy for atherosclerotic renal artery stenosis. Circulation. 2006;113(11):1464-1473.
- Zeller T, Frank U, Muller C, et al. Predictors of improved renal function after percutaneous stent-supported angioplasty of severe atherosclerotic ostial renal artery stenosis. Circulation. 2003;108(18):2244-2249.
- Burket MW, Cooper CJ, Kennedy DJ, et al. Renal artery angioplasty and stent placement: predictors of a favorable outcome. Am Heart J. 2000;139(1 Pt 1):64-71.
- Bax L, Woittiez AJ, Kouwenberg HJ, et al. Stent placement in patients with atherosclerotic renal artery stenosis and impaired renal function: a randomized trial. Ann Intern Med. 2009;150(12):840-848.
- Wheatley K, Ives N, Gray R, et al. Revascularization versus medical therapy for renal-artery stenosis. N Engl J Med. 2009;361(20):1953-1962.
- Tsao CR, Liu TJ, Chen FC, et al. Intravenous aminophylline provides no additional renal protection in patient with severe atherosclerotic renal artery stenosis treated by delicate percutaneous renal intervention. Int J Cardiol. 2006;110(1):122-124.
- Cicuto KP, McLean GK, Oleaga JA, Freiman DB, Grossman RA, Ring EJ. Renal artery stenosis: anatomic classification for percutaneous transluminal angioplasty. AJR Am J Roentgenol. 1981;137(3):599-601.
- Kaatee R, Beek FJ, Verschuyl EJ, et al. Atherosclerotic renal artery stenosis: ostial or truncal? Radiology. 1996;199(3):637-640.
- Rihal CS, Textor SC, Breen JF, et al. Incidental renal artery stenosis among a prospective cohort of hypertensive patients undergoing coronary angiography. Mayo Clin Proc. 2002;77(4):309-316.
- Park S, Jung JH, Seo HS, et al. The prevalence and clinical predictors of atherosclerotic renal artery stenosis in patients undergoing coronary angiography. Heart Vessels. 2004;19(6):275-279.
- Marcantoni C, Rastelli S, Zanoli L, et al. Erratum to: Prevalence of renal artery stenosis in patients undergoing cardiac catheterization. Intern Emerg Med. 2011 Jun 26 (Epub ahead of print).
- Crowley JJ, Santos RM, Peter RH, et al. Progression of renal artery stenosis in patients undergoing cardiac catheterization. Am Heart J. 1998;136(5):913-918.
- Rimoldi SF, Yuzefpolskaya M, Allemann Y, Messerli F. Flash pulmonary edema. Prog Cardiovasc Dis. 2009;52(3):249-259.
- Lao D, Parasher PS, Cho KC, Yeghiazarians Y. Atherosclerotic renal artery stenosis — diagnosis and treatment. Mayo Clin Proc. 2011;86(7):649-657.
- Strandness DE Jr. Natural history of renal artery stenosis. Am J Kidney Dis. 1994;24(4):630-635.
- Chrysochou C, Kalra PA. Epidemiology and natural history of atherosclerotic renovascular disease. Prog Cardiovasc Dis. 2009;52(3):184-195.
- Hirsch AT, Haskal ZJ, Hertzer NR, et al. ACC/AHA Guidelines for the Management of Patients with Peripheral Arterial Disease (lower extremity, renal, mesenteric, and abdominal aortic): a collaborative report from the American Associations for Vascular Surgery/Society for Vascular Surgery, Society for Cardiovascular Angiography and Interventions, Society for Vascular Medicine and Biology, Society of Interventional Radiology, and the ACC/AHA Task Force on Practice Guidelines (writing committee to develop guidelines for the management of patients with peripheral arterial disease) — summary of recommendations. J Vasc Interv Radiol. 2006;17(9):1383-1397.
- Shetty R, Biondi-Zoccai GG, Abbate A, Amin MS, Jovin IS. Percutaneous renal artery intervention versus medical therapy in patients with renal artery stenosis: a meta-analysis. EuroIntervention. 2011;7(7):844-851.
- Rimmer JM, Gennari FJ. Atherosclerotic renovascular disease and progressive renal failure. Ann Intern Med. 1993;118(9):712-719.
- Dorros G, Jaff M, Mathiak L, et al. Four-year follow-up of Palmaz-Schatz stent revascularization as treatment for atherosclerotic renal artery stenosis. Circulation. 1998;98(7):642-647.
- Harden PN, MacLeod MJ, Rodger RS, et al. Effect of renal-artery stenting on progression of renovascular renal failure. Lancet. 1997;349(9059):1133-1136.
- Beutler JJ, Van Ampting JM, Van De Ven PJ, et al. Long-term effects of arterial stenting on kidney function for patients with ostial atherosclerotic renal artery stenosis and renal insufficiency. J Am Soc Nephrol. 2001;12(7):1475-1481.
- Lederman RJ, Mendelsohn FO, Santos R, Phillips HR, Stack RS, Crowley JJ. Primary renal artery stenting: characteristics and outcomes after 363 procedures. Am Heart J. 2001;142(2):314-323.
- Ramos F, Kotliar C, Alvarez D, et al. Renal function and outcome of PTRA and stenting for atherosclerotic renal artery stenosis. Kidney Int. 2003;63(1):276-282.
- Rocha-Singh K, Jaff MR, Rosenfield K. Evaluation of the safety and effectiveness of renal artery stenting after unsuccessful balloon angioplasty: the ASPIRE-2 study. J Am Coll Cardiol. 2005;46(5):776-783.
- Holden A, Hill A, Jaff MR, Pilmore H. Renal artery stent revascularization with embolic protection in patients with ischemic nephropathy. Kidney Int. 2006;70(5):948-955.
- Paul TK, Lee JH, White CJ. Renal embolic protection devices improve blood flow after stenting for atherosclerotic renal artery stenosis. Catheter Cardiovasc Interv. 2012;80(6):1019-1022.
- Kumbhani DJ, Bavry AA, Harvey JE, et al. Clinical outcomes after percutaneous revascularization versus medical management in patients with significant renal artery stenosis: a meta-analysis of randomized controlled trials. Am Heart J. 2011;161(3):622.e1-630.e1.
- Rimoldi SF, de Marchi SF, Windecker S, Meier B, Allemann Y. Screening renal artery angiography in hypertensive patients undergoing coronary angiography and 6-month follow-up after ad hoc percutaneous revascularization. J Hypertens. 2010;28(4):842-847.
From the Cardiovascular Center, Taichung Veterans General Hospital, Taichung, Taiwan and the Institute of Clinical Medicine, Cardiovascular Research Center, and Department of Medicine, National Yang Ming University School of Medicine, Taipei, Taiwan.
Funding: This study was supported in part by the Yen Tjing-Ling Medical Foundation (CI-100) and grants from Taichung Veterans General Hospital (TCVGH-996301C and TCVGH-993106C) in Taichung, Taiwan.
Disclosure: The authors have completed and returned the ICMJE Form for Disclosure of Potential Conflicts of Interest. The authors report no conflicts of interest regarding the content herein.
Manuscript submitted October 22, 2012, provisional acceptance given December 4, 2012, final version accepted February 6, 2013.
Address for correspondence: Wen-Lieng Lee, MD, PhD, Cardiovascular Center, Taichung Veterans General Hospital, 160, Sec. 3, Chung-Kang Road, Taichung 407, Taiwan. Email: email@example.com