Effects of Global Renal Artery Stenting on Chronic Renal Failure
- Fri, 9/5/08 - 3:36pm
- 0 Comments
- 3483 reads
Roberto Rivolta, MD, Claudio Bazzi, MD, Paola Stradiotti, MD
Introduction
The natural history of atherosclerotic renal artery stenosis is characterized by progression, causing hypertension and chronic renal failure (RF). Up to 21% of patients with renal stenosis reducing luminal diameter by more than 60% progress to occlusion within 2 years. Renal stenosis is responsible for renal failure in 15% of adult patients who begin dialysis each year.1–3
Renal angioplasty4 with renal artery stenting (RAS)5–8 has become the procedure of choice in the treatment of stenosis. The technical success and low complication rates after percutaneous balloon angioplasty and stenting of renal stenosis have been widely published,9,10 but despite these favorable reports, the ability of revascularization to improve the function of the treated kidney has not been clearly demonstrated.11–13
As underlined by some researchers,11,14–15 it is difficult to study the direct effect of treatment upon a single kidney because we lack simple methods to assess split function in this normally paired organ system. Serum creatinine is the more accepted method to evaluate RF, but reflects the function of the normal bilateral organs. Thus, in unilateral renal artery stenosis, an abnormal creatinine level suggests dysfunction of the contralateral “non-stenosed” kidney and obscures the direct effect of treatment of unilateral disease. To overcome this problem and isolate the direct effects of stenting, we studied a group of patients that presented stenoses of all remaining renal arteries (global renal ischemia). We evaluated the effects of stenting on overall RF during a medium-term period, using a longitudinal method to establish effective change in RF (i.e., slopes of reciprocal of creatinine over time).
Subjects and Methods
Patient selection. All patients with renal artery stenosis, presenting through the nephrological and radiological departments, were evaluated for inclusion. Patients were considered eligible if they had a chronic renal impairment (serum creatinine > 1.5 mg/dL) and atherosclerotic renovascular disease with demonstrable stenosis (> 70% luminal diameter established by angiography with aid of a quantitative computerized software). Significant stenosis had to involve all renal arteries or, if the patients had unilateral stenosis, it must be in the setting of a solitary or single functional kidney. A nonfunctional kidney was defined as one being atrophic (pole-to-pole length < 7.5 cm).8 Patients with artery stenosis involving only one of two functioning kidneys were excluded because of the difficulty in establishing the cause for change in overall RF after unilateral intervention in these patients.
Procedure. Angiography, angioplasty and RAS were usually performed transfemorally (in two cases transaxillary). Heparin was administered (3000–5000 U) during the procedure, before angioplasty. To minimize contrast dose and reduce catheter manipulation, the renal arteries were localized by use of a pigtail catheter in the aorta, and flush injections of contrast diluted 1:1 with normal saline were used. During the stenting procedure, mean radiographic contrast dose was 48 ± 12 mL for the kidney.
Only subocclusive stenoses were predilatated with balloon catheters. We usually performed direct stenting utilizing premounted stents (Corinthian and Genesis, Cordis Corporation, Miami Lakes, Florida or Express South Dakota, Boston Scientific Corporation, Maple Grove, Minnesota), with diameters ranging from 4–6 mm. In initial cases (n = 6), nonarticulated Palmaz stents (Cordis Endovascular, Warren, New Jersey) were mounted on appropriately-sized balloon catheters (5–7 mm) and deployed at 8–12 atm.
After stenting was performed, aspirin (325 mg daily) was continued indefinitely.
Follow-up. The primary endpoint of the study was to assess the changes of RF before and after stenting by comparing the slopes of the reciprocal of serum creatinine versus time. Patients were evaluated at 1, 3, 6, 9 and 12 months, and every 6 months thereafter. Review involved clinical examination and measurement of serum creatinine. Follow-up was considered adequate only if at least 5 serum creatinine measurements were available during a post-stent 9-month period. Only patients with adequate prior documentation of the course of RF were included in this study, i.e., patients having at least 5 values of serum creatinine during the previous 6-month period.
Renal color Doppler ultrasonography was performed at baseline at 1 and 6 months, and then yearly. Renal size (RS), assessed by ultrasonographic measurement of pole-to-pole length, and peak systolic velocity, measured along the trunk of renal artery and in the intra-stent segment, was evaluated. The effect of RS on renal dimension was assessed by comparing baseline with final follow-up kidney length. According to other authors,8 atrophy was defined as a reduction > 1 cm in kidney length during follow-up; a nonfunctional kidney was defined as one being atrophic (long diameter < 7.5 cm) and with an occluded or small, diffusely diseased renal artery. Resistive index (RI), measured on interlobar artery of treated kidneys, was also obtained. Complete technique of echo-Doppler examination of kidney is described elsewhere.16 Restenosis (> 70%) was suggested by a value of intra-stent or extra-stent velocity > 180 cm/s. In this case, angiography and angioplasty were performed.
1. Caps MT, Zierler RE, Polissar NL, et al. Risk of atrophy in kidneys with atherosclerotic renal artery stenosis. Kidney Int 1998;53:735–742.
2. Van Ampting JMA, Penne EL, Beek FJA, et al. Prevalence of atherosclerotic renal artery stenosis in patients starting dialysis. Nephrol Dial Transplant 2003;18:1147–1151.
3. Fatica RA, Port FK, Young EW. Incidence trends and mortality in end-stage renal disease attributed to renovascular disease in the United States. Am J Kidney Dis 2001;37:1184–1190.
4. Martin LG, Cork RD, Kaufman SL. Long-term results of angioplasty in 110 patients with renal artery stenosis. J Vasc Interv Radiol 1992;3:619–626.
5. Rundback JH, Jacobs JM. Percutaneous renal artery stent placement for hypertension and azotemia: A pilot study. Am J Kidney Dis 1996;28:214–219.
6. Blum U, Krumme B, Flugel P, et al. Treatment of ostial renal artery stenoses with vascular endoprostheses after unsuccessful balloon angioplasty. N Engl J Med 1997;336:459–465.
7. Dorros G, Jaff M, Mathiak L, et al. Four-year follow-up of Palmaz Schatz stent revascularization as a treatment for atherosclerotic renal artery stenosis. Circulation 1998;98:642–647.
8. Watson PS, Hadjipetrou P, Cox SV, et al. Effect of renal artery stenting on renal function and size in patients with atherosclerotic renovascular disease. Circulation 2000; 102: 1671-1684.
9. Dorros G, Jaff M, Mathiak L, He T. Multicenter palmaz stent renal artery stenosis revascularization registry report: Four years follow-up of 1058 successful patients. Catheter Cardiovasc Interv 2002;55:182–188.
10. Leertouwer TC, Gussenhoven EJ, Bosch JL, et al. Stent placement for renal arterial stenosis: Where do we stand? A meta-analysis. Radiology 2000;216:78–85.
11. Morganti A, Bencini C, Del Vecchio C, Strata M. Treatment of atherosclerotic renal artery stenosis. J Am Soc Nephrol 2002;13:S187–S189.
12. Middleton JP. Ischemic disease of the kidney: How and why to consider revascularization. J Nephrol 1998;11:123–136.
13. Rees CR. Stent for atherosclerotic renovascular disease. J Vasc Int Rad 1999;10:689–705.
14. Safian RD, Textor SC. Medical progress: Renal artery stenosis. N Eng J Med 2001;344:431–442.
15. Coen G, Moscaritolo E, Catalano C, et al. Atherosclerotic renal artery stenosis: One-year outcome of total and separate kidney function following stenting. BMC Nephrology 2004;5:15–23.
16. Rivolta R, Cardinale L, Lovaria A, et al. Variability of renal echo-Doppler measurements in healthy adults. J Nephrol 2000;13:110–115.
17. Mitch WE, Walser M, Buffington GA, Lemann J Jr. A simple method of estimating the progression of chronic renal failure. Lancet 1976;2:1326–1328.
18. 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;19:250–271.
19. Mailloux LU, Napolitano B, Bellucci AG, et al. Renal vascular disease causing end stage renal disease, incidence, clinical correlates and outcome: A 20 year experience. Am J Kidney Dis 1994;24:622–629.
20. Harden PN, Macleod MJ, Rodger RSC, et al. Effect of renal artery stenting on progression of renovascular renal failure. Lancet 1997;349:1133–1136.
21. 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;108:2244–2249.
22. Haller C. Arteriosclerotic renal artery stenosis: Conservative versus interventional management. Heart 2002;88:193–197.
23. Radermacher J, Chavan A, Bleck J, et al. Use of Doppler ultrasonography to predict the outcome of therapy for renal artery stenosis. N Engl J Med 2001;344:410–417.
24. van Jaarsveld BC, Krijnen P, Pieterman H, et al. 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.
25. Bax L, Mali W, Buskens E, et al. The benefit of stent placement and blood pressure and lipid-lowering for the prevention of progression of renal dysfunction caused by Atherosclerotic ostial stenosis of the renal artery. The STAR-study: Rationale and study design. J Nephrol 2003;16:807–812.










Post new comment