The progressive nature of atherosclerotic renal artery stenosis is now well recognized.1–8 Observational data suggests that untreated renal artery stenosis can lead to progressive hypertension, renal insufficiency, and increased mortality.6,9–11 The incidence of progressive ischemic nephropathy resulting from atherosclerotic renal artery stenosis had been underestimated in the past. The U.S. Renal Data System annual report in 1999 revealed that up to 20% of new patients > 50 years old requiring hemodialysis have underlying renovascular disease.12 Medical management of hypertension associated with renal artery stenosis mainly focuses on blood pressure control. Despite reports that surgical revascularization can improve blood pressure, delay the progression of renal failure or even reverse it in some patients,13-20 it has been reserved for patients refractory to medical management. This is mainly due to the fact that aorto-renal bypass carries with it a high morbidity and mortality (rates up to 6–8%).16,21–25 In the last 2 decades, percutaneous revascularization with angioplasty and more recently, stenting has offered the benefit of revascularization with significantly reduced morbidity, mortality and in-hospital stay. Observational studies have reported improvement in blood pressure in a large proportion of the patients following renal artery stenting. However, the literature regarding the effect of renal artery stenting on renal function reveals conflicting results. Some authors report improved renal function in 40–100% of patients26–38 while others found no significant impact of revascularization on renal function.3,39–47 Others have even reported worsening of renal function following renal angiography or percutaneous revascularization in 10–40% of patients, some of them subsequently requiring hemodialysis.33,45,47–49 The purpose of this retrospective study is to evaluate the long-term effect of renal artery stenting (performed primarily for suspected renovascular hypertension) on renal function in patients with atherosclerotic renal artery stenosis (> 70% diameter stenosis). Methods This is a retrospective analysis of 72 consecutive patients who underwent renal artery stenting, primarily for renovascular hypertension, at a single institution. All patients had drug refractory hypertension (defined as systolic blood pressure > 140 mmHg and diastolic blood pressure > 90 mmHg despite 2 antihypertensive drugs) and > 70% diameter stenosis in one or both renal arteries. Unilateral renal artery stenting was performed in 54 patients (54/72 = 75%) and bilateral stenting in 18/72 (25%). Definitions. Acute procedural success was defined as = 1.5 mg/dl. “Improvement” in renal function was defined as decrease in serum creatinine by >= 20% compared to baseline. Renal function was considered “unchanged” if creatinine varied by = 20%. Serum creatinine levels were followed on an out-patient basis at the clinician’s discretion. Serum creatinine was evaluated at approximately 6 months, 1, 2 and 3 years post-renal artery stenting for eligible patients. Since there was no significant variation in the interim mean values, the latest serum creatinine values are presented. Paired t-test was used for validation of this comparison. A p value = 1.5 mg/dl). The renal function “improved” in 3 patients (3/17 = 18%, 2.7 ± 1 to 1.6 ± 0.6 mg/dl, p = ns), remained “unchanged” in 9 patients (9/17 = 53%), and was “worse” in 5 patients (5/17 = 29%, 2 ± 0.51 to 3.3 ± 0.34 mg/dl, p = 0.005) but none of them required hemodialysis. Seven patients (7/70 = 10%) had clinical restenosis, (3 bilateral and 4 unilateral) requiring repeat renal revascularization. Four of these patients (4/7 = 57%) had abnormal baseline creatinine and remained “unchanged” at follow-up. Three patients (3/7 = 43%) had normal baseline creatinine and remained normal at follow-up. The characteristics of the patients who experienced worsening of renal function at follow-up (with either normal or abnormal baseline creatinine) were similar to the characteristics of the total cohort (Table 3). Discussion Atherosclerotic renal artery stenosis is a progressive disease and if untreated, may lead to renal dysfunction (ischemic nephropathy) often requiring hemodialysis.1–11 Surgical revascularization can delay the progression of renal failure, and in some cases reverse it, but is associated with high procedural morbidity and mortality.13–25 While several retrospective studies have reported sustained hemodynamic benefits of relieving renal artery obstruction,50–52 the role of percutaneous renal artery revascularization to prevent, arrest or reverse ischemic nephropathy is much less defined. Dorros et al. have reported the largest series of patients (163 at a single institution and a multi-center registry of 1,058 patients) with up to 4-year follow-up. They found improvement or stabilization of renal function in up to two-thirds of the patients.27,28 A number of other studies report improvement or stabilization of renal function ranging from 40–100% of patients following percutaneous renal artery revascularization.26,29–38 On the contrary, some authors have reported significant worsening of renal function following renal stenting (in up to 10–40% of patients, with only a few requiring hemodialysis).33,45,47–49 This has attributed to athero-embolism or contrast nephropathy, and in the long term, to progression of diabetes or uncontrolled hypertension. In our group of patients who underwent revascularization of significant renal artery stenosis, primarily for suspected renovascular hypertension, we found that renal function remained stable in 89% of patients (54/61) and worsened in 11% (7/61) patients at 2-year follow-up. In patients with a baseline serum creatinine of 1.5 mg/dl, the renal function remained stable in 71% of them at follow-up. Despite clinical restenosis in 7 patients (7/70 = 10%), the serum creatinine remained unchanged in this group. It is possible that repeat renal revascularization contributed to maintaining stability of renal function. Two patients (2/70 = 3%) with normal baseline creatinine had worse creatinine at follow-up. This was not likely to be secondary to the use of radio-contrast or atheroembolism since the elevation in creatinine was seen late in follow-up. These 2 patients did not have clinical restenosis and had normal blood pressure at follow-up. Study limitations. 1) This is a retrospective analysis with a mean follow-up of approximately 2 years. A prospective evaluation with longer follow-up is desirable. 2) Serum creatinine was used as the marker of renal function. More accurate ways to quantify renal function, like glomerular filtration rate or nuclear renal scans were not used. 3) A serum creatinine of > 1.5 mg/dl was used to define abnormal renal function. This was not adjusted for body size. 4) Nine of the 70 eligible patients (13%) were lost to follow-up. A complete follow-up would be desirable. Conclusions In patients with atherosclerotic renal artery stenosis treated using renal artery stenting, the renal function remained stable in 89% of patients and worsened in 11% of patients at 21 months (follow-up was available in 87% of the eligible patients). In patients with baseline renal insufficiency (serum creatinine > 1.5 mg/dl), the renal function remained stable in 71% of patients.
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