Percutaneous stenting of atherosclerotic ostial renal artery stenosis

Cardiology Review® Online, November 2004, Volume 21, Issue 11

Renal artery stenosis is a progressive disease involving the origin of the vessel, frequently occurring in patients with atherosclerosis.1 Kidney hypoperfusion causes poorly controllable hypertension and chronic renal failure due to hypertensive or ischemic nephropathy.2 Stent-supported percutaneous transluminal renal angioplasty has become an established treatment option that has been investigated in various studies.2-6 The effect of percutaneous renal revascularization on preservation of renal function, however, is still a matter of debate.2,5,7,8 The aim of this prospective study was to identify characteristics that could predict or preclude improvement of renal function during a 1-year follow-up period in a large cohort of patients undergoing stent placement for severe ostial renal artery stenosis.

Patients and methods

The study included 215 consecutive patients with 277 ostial renal artery stenoses, representing 91% of all patients undergoing stent placement for arteriosclerotic renal lesions located within 1 cm of the origin during a 5-year period. In most cases, assessment of renal artery stenosis was primarily based on duplex ultrasound.6,9 Before intervention, duplex ultrasound was always confirmed by angiography, showing a percent diameter stenosis of at least 70% on visual estimation. Indications for renal percutaneous stenting were hypertension (World Health Organization grade 1 or higher regardless of concomitant therapy) or impaired renal function (serum creatinine concentration > 1.1 mg/dL in women and > 1.2 mg/dL in men), or both.

We excluded patients who had been on a hemodialysis program for longer than 1 year and patients who had had interventions in chronically occluded arteries. The guiding catheter technique and the procedure for implantation of the various types of stents have been described previously.10 In 50 patients (23%), bilateral stenoses were treated simultaneously.

The end point of the study was the proportion of patients with decreased serum creatinine within 1 year of study entry (serum creatinine at 1 year less than baseline serum creatinine). Analysis was by intention to treat. The last creatinine measurement before entering the hemodialysis program was taken as the baseline for patients who were included in a hemodialysis program during the study period. For those who were withdrawn from a hemodialysis program, follow-up creatinine concentration was recorded. The creatinine clearance calculated by the Cockroft-Gault formula was also analyzed.

Logistic regression analysis was performed to identify independent predictors for the study end point. The following variables were en-

tered into the model: age; sex; baseline serum creatinine concentration; baseline mean blood pressure; left ventricular function; diameter stenosis of 90% or greater; resistance index greater than 0.80 after inter-

vention; parenchymal/pelvic ratio greater than 1 for the affected kidney; bilateral stenosis; diabetes mellitus; concomitant atherosclerotic disease, such as coronary disease, peripheral occlusive disease, and cerebral occlusive disease; dyslipidemia; obesity; and smoking. Two-tailed hypothesis testing was used. Statistical significance was considered P < .05.


Intervention was successful for all 215 patients. Severe procedure-related adverse events occurred in six patients (2.8%), including progression from preterminal renal failure to terminal renal failure due to renal embolism and dye-induced nephropathy (in four patients). During the follow-up period, 16 patients died, resulting in a 1-year mortality rate of 7.4%. Twelve patients (73%) died from cardiac causes; cerebral incidents occurred in two patients (13.5%); and malignancy occurred in two patients (13.5%). Eight patients were lost to follow-up, leaving 191 patients with 249 treated lesions available for 1-year follow-up. One year after entry into the study, 28 (11.2%) of the 249 renal arteries developed restenosis.

Mean serum creatinine concentrations decreased significantly from 1.21 mg/dL (quartiles: 0.92 mg/dL, 1.60 mg/dL) at baseline to 1.10 mg/dL (quartiles: 0.88 mg/dL, 1.50 mg/dL) at 1 year (P = .047). Reduction in serum creatinine concentration over the 1-year follow-up period was reached in 99 of 191 patients (52%). In seven patients hospitalized with flash pulmonary edema or acute renal failure requiring acute hemodialysis, or both, hemodialysis could be discontinued. The median reduction in serum creatinine concentration was 0.02 mg/dL (quartiles: —0.11 mg/dL, 0.23 mg/dL,

P = .011) at the 1-year follow-up. Creatinine clearance was also significantly increased, by 2.3 ± 15.1 mL/min (P = .028). The same outcome, with a median decrease in serum creatinine concentration of 0.02 mg/dL (quartiles: —0.10 mg/dL, 0.25 mg/dL, P = .001), was obtained when the last available serum creatinine concentration determination for patients who were lost to follow-up or died was included.

Patients with improved renal function showed a median decrease in serum creatinine concentration of 0.22 mg/dL (quartiles: 0.12 mg/dL, 0.39 mg/dL). There was a median increase of 0.11 mg/dL (quartiles: 0.05 mg/dL, 0.23 mg/dL) in those patients who did not have improved renal function.

Patients with impaired renal function at study entry (creatinine > 1.5 mg/dL; n = 48) had a significant median decrease in serum creatinine concentration of 0.33 mg/dL (quartiles: —0.01 mg/dL, 0.67 mg/dL, P = .025), whereas those with normal renal function (creatinine > 1.5 mg/

dL; n = 143) had no significant change in serum creatinine concentration (median, 0.01 mg/dL [quartiles: —0.11 mg/dL, 0.14 mg/dL]). This difference between the two groups defined by the 1.5 mg/dL cutoff for serum creatinine was statistically significant at P < .001. In general, the higher the decrease in serum creatinine concentration, the more severe impaired renal function was at baseline (figure 1).

There was no significant difference in baseline characteristics, except baseline serum creatinine, between the two groups. Decreases in serum creatinine concentration similar to the decrease in the entire cohort were found in patients with diabetes mellitus (0.05 mg/dL [quartiles: —0.11 mg/dL, 0.30 mg/dL]), severe nephrosclerosis (0.09 mg/

dL [quartiles: —0.09 mg/dL, 0.21 mg/dL]), and unilateral involvement (0.01 mg/dL [quartiles: –0.11 mg/dL, 0.21 mg/dL], P = .047). Baseline serum creatinine concentration (P = .004) and left ventricular function (P = .032) were significant independent predictors for the decrease in serum creatinine at 1 year (figure 2).


Slowing the decline in renal function is sufficient to claim a benefit from renal artery angioplasty according to the guidelines of the American Heart Association.11 This study showed significant improvement in renal function 1 year after intervention. Thus, our findings provide a conservative estimate of the advantages of renal angioplasty using stents. Impaired left ventricular function and increased serum creatinine were independent predictors of improved renal function. Nephrosclerosis and diabetes mellitus were not associated with a poor outcome in renal function. Furthermore, unilateral and bilateral treatment were associated with improvement of renal function.

Other studies have not shown marked improvement of renal function after angioplasty of renal artery stenosis. The Dutch Renal Artery Stenosis Intervention Cooperative (DRASTIC) study was the only randomized trial to compare medical treatment with balloon angioplasty of atherosclerotic renal artery stenosis.12 That study did not show improved renal function after angioplasty. The interpretation of the study, however, is hindered by an outmoded interventional procedure with a 44% restenosis rate and a large percentage of crossover patients. Plain balloon angioplasty has been replaced by stent-supported angioplasty for atherosclerotic ostial renal artery stenosis because stenting provides outstanding acute and long-term results.13 Several studies, however, have not shown any marked improvement in serum creatinine concentrations with stenting.3,7 These differing results may be because of a small sample size and because a considerable number of patients in earlier studies had 50% to 70% stenoses, which were not likely to cause hemodynamic compromise.7,8,12,13 The results of our study, which had a sufficient sample size, showed improved renal function comparable with that shown in other studies.4,5,14 The favorable outcome of the present study may have been the result of using percutaneous stenting as the treatment.

This study shows that more patients can benefit from stent-supported renal angioplasty than originally believed, especially patients with nephrosclerosis and diabetes mellitus. Radermacher and colleagues, however, found no improvement from renal artery revascularization in patients with severe nephrosclerosis.8 The difference between their study and ours may be that the majority of patients in their study were treated with plain balloon angioplasty.

Contrary to earlier studies, the results achieved from the intervention were not related to bilateral stenoses in our study.4,5,8,14 The patients who showed the greatest improvement in renal function had congestive heart failure and renal insufficiency. If there is a concomitant systemic prerenal component or if the hemodynamic compromise is serious enough to result in renal dysfunction, improvement in renal artery stenosis may be most effective.

This study was limited by the lack of a control group. Although progressive renal failure is a result,of severe renal artery stenosis,2 our study showed that the process can be prevented by angioplasty with stenting. The advantages of endovascular treatment of renal artery stenosis over conservative treatment, however, require further study. The benefit of stent-supported angioplasty in patients without renal dysfunction may have been underestimated in our study. Angioplasty may halt decline in renal function in these patients, but it is a benefit that does not become evident without a control group.


Percutaneous stenting for serious ostial renal artery stenosis improved blood pressure and renal function in a larger range of patients than was formerly believed. Patients with

diabetes mellitus, nephrosclerosis, and unilateral involvement should not be prevented from undergoing stent-supported angioplasty. Patients with left ventricular dysfunction or those who already had renal dysfunction received the greatest improvement in renal function from stent-supported angioplasty.