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World J Nephrol. Sep 25, 2026; 15(3): 124524
Published online Sep 25, 2026. doi: 10.5527/wjn.124524
Table 1 Major studies on renal artery stenting since 2016
Ref.
Study size and type
Baseline stenosis
Baseline blood pressure (mmHg) and anti-hypertensives
Baseline kidney function
Inclusion/exclusion criteria
Findings
Warfield et al[23], 2026 and Warfield et al[24], 2025Single center, retrospective; 99 patients85% patients with ≥ 70% and 60% of patients with ≥ 90% stenosis165 ± 23/80 ± 14; 3.4 ± 1.3 medicationsGFR: Mean = 39, SD = 24Exclusion: FMD, transplant renal artery, ADPKD. Inclusion: Renal artery stent in at least one artery from January 2004 to December 2023Renal artery stenting decreased both systolic and diastolic BP for five years. Defined daily dose and antihypertensive medication counts were decreased for 3 years and returned to baseline at 5 years post-stenting. Diastolic HTN (≥ 80 mmHg) and rapidly increasing blood pressure (≥ 15 mmHg increase over one year prior to stenting) were independently associated with larger decreases in systolic BP after stenting. ≥ 90% stenosis was a positive effect modifier for patients with only one of these predictors. Patients with neither predictor, one predictor, one predictor and ≥ 90% stenosis, or both predictors were progressively more likely to experience ≥ 20 mmHg decrease in systolic BP at 3 months post-stenting. GFR and serum creatinine increased from one year prior to stenting to time of stent placement and then decreased for five years after stenting in patients with rapidly declining kidney function (GFR decline of ≥ 5 mL/minute per 1.73 m2 within a year prior to stenting). This same pattern was seen in the overall cohort but was not significant. Both rapidly declining kidney function and ≥ 90% stenosis independently correlated with GFR improvement after stenting. Single functioning kidney was a positive effect modifier for patients with both predictors. Patients with neither predictor, one predictor, both predictors, or both predictors and single functioning kidney had progressively greater chance of ≥ 20% GFR increase following stenting
Modrall et al[33], 2017Single center, retrospective; 61 patientsN/AMedian: 149/75; IQR: 140-179/67-89; on median 4 (IQR: 3-5) medicationsGFR: Median = 34, IQR = 24-45Serum creatinine > 1.5 at baselinePatients after stenting were grouped as “responders” if eGFR increased by 20%. Responders had improved overall survival compared to non-responders. There were 17 responders and 44 non-responders of 61 included patients. The only significant independent predictor of being a responder was more rapid decline in kidney function. Responders had a median of -2.1% decline in GFR (IQR: -3.8% to -1%) per week whereas non-responders had median 0% (IQR: -0.8% to 1.4%) GFR decline per week prior to stenting
Modrall et al[30], 2023Post-hoc analysis of CORAL trial67.3% ± 11.4%149.9 ± 23.2 on 2.1 medicationsGFR: Mean = 58.0, SD = 23.4CORAL patientsCORAL post-hoc analysis which showed that the stent plus medical therapy group had significantly more responders (classified as GFR improvement > 20% after stenting). Event free survival was significantly better for responders. However, only 25.6% of stent plus medical therapy patients were responders vs 17.1% of medical therapy patients being responders. Diabetes was a negative predictor of improved renal function after stenting and higher urine albumin creatinine ratio correlated with lower event free survival and worsened renal function
Modrall et al[22], 2020Post-hoc analysis of CORAL trial67.3% ± 11.4%Systolic: Mean = 149.9, SD = 23.2; 2.1 medicationsGFR: Mean = 58.0, SD = 23.4CORAL patientsPatients were categorized as responders if their post-stenting BP was < 160/90 mmHg with fewer meds or diastolic < 90 mmHg. Predictors of this response were pre-stenting diastolic BP > 90 mmHg, clonidine use, and ≥ 4 anti-hypertensive medications. Responders and non-responders did not differ in event free survival. Percent of positive responders increased as the number of pre-procedural predictors increased
Modrall et al[32], 2023VA database of 40 VA centers, retrospective; 695 patientsN/AMedian = 145/74, IQR = 133-161/67-81GFR: Median = 46.0, IQR = 34.0-61.6VA patients stented from 2000 to 2021Overall, these VA patients had lower systolic and diastolic BP requiring the same number of medications with similar GFR. Responders (defined as GFR increase > 20% after stenting) had a 26.1% increase in GFR which was maintained throughout an average of 7.1 years of follow-up. Predictors of being a responder were CKD 3b and 4 (as opposed to stage 1, 2, 3a, and 5), more rapid decline in GFR, and diabetes (which had a negative correlation)
Courand et al[17], 2019Single center, retrospective; 72 patients78% ± 10%157 ± 16/82 ± 10; 4.0 ± 1.0 medicationsGFR: Mean = 52, SD = 11Resistant HTN (SBP > 135 or DBP > 85 mmHg despite at least 3 antihypertensive drugs, including a diuretic)Renal angioplasty (stenting in 66/72 patients) decreased daily ambulatory BP and anti-hypertensive burden but had no effect on GFR in patients with resistant HTN (defined as > 135 mmHg SBP or > 85 mmHg DBP despite 3 antihypertensive medications including one diuretic). High baseline SBP and low BMI predicted good response. These data were at first follow-up (mean = 57 days after stenting). Subset of patients at 1 year (n = 31) and 3 years (n = 18) showed similar results. Higher SBP, lower BMI, younger age, and higher GFR prior to stenting predicted lower post-stenting BP
Edgar et al[20], 2023Three centers, retrospective; 72 patientsN/A187 ± 30/89 ± 19GFR: Median = 25, IQR = 8-42All patients who had been stented72 patients stratified by indication (HTN, renal dysfunction, or pulmonary edema). HTN and medication burden improved at one-year post-stenting without worsening kidney function. Intervention for kidney dysfunction led to improved GFR at 6-months post-stenting. Intervention for pulmonary edema was universally successful. Patients who would have been excluded from the CORAL trial but were included in this trial had greater reduction in serum creatinine and an equivalent reduction in SBP
Murphy et al[35], 2016Post hoc analysis of CORAL trial67.3% ± 11.4%149.9 ± 23.2; 2.1 medicationsGFR: Mean = 58.0, SD = 23.4CORAL patientsPre-stenting albuminuria < 22.5 mg/g (median baseline UACR of all CORAL patients) was associated with improved event free survival at five years in the stent plus medical therapy group as compared to the medical therapy group. This was true of the composite end point, cardiovascular disease related death, progressive renal insufficiency, and overall survival. Group with albuminuria was > 22.5 prior to randomization saw no difference in outcomes following either stenting plus medical therapy or medical therapy alone
Reinhard et al[16], 2022 (DAN-PTRA trial)Two centers, prospective; 102 patients40% of patients with ≥ 90% stenosis166.2 ± 21.6/82.3 ± 12.3; 4 (3.7-4.2) antihypertensivesMedian = 39.7, IQR = 23.5- 54.0Stenosis > 70% plus resistant HTN (ambulatory SBP > 130 despite 3 meds 1 of which is diuretic), rapidly declining kidney function (reduction in GFR > 5 mL/minute per year), or recurrent heart failure (2 hospital admissions)/flash pulmonary edema (1 hospital admission) without another explanation such as left ventricular ejection fraction < 40%Prospective study of patients with stenosis > 70% plus one or more of; resistant HTN (defined as SBP > 130 mmHg despite 3 antihypertensive medications, 1 of which is a diuretic), rapidly declining kidney function (defined as a reduction in GFR > 5 mL/minute per year), or recurrent heart failure (defined as at least 2 hospital admissions)/flash pulmonary edema (only 1 hospital admission) without another explanation such as a left ventricular ejection fraction < 40%. This study found lower BP and lower antihypertensive burden and higher GFR (in RDKF patients). UACR was also found to have increased over the year before stenting and then decreased over the year after stenting which was maintained for 3 years. High baseline ambulatory SBP, younger age, and recent angiotensin converting enzyme/angiotensin receptor blocker discontinuation predicted good a BP response. Female sex, high baseline ambulatory SBP, RDKF, recurrent heart failure/pulmonary edema, and stenosis > 90% predicted an improvement in GFR at 3 months
Vassallo et al[34], 2018Singel center, retrospective; 263 patientsAll patients with > 70% stenosisMedian = 155/80, IQR = 134-180/69-88GFR: Median = 29.5, IQR = 20.4-41.3≥ 70% unilateral or bilateral stenosis with or without high-risk features defined as: (1) FPE or acute decompensated HF without known left ventricular ejection fraction < 40%; (2) Systolic BP ≥ 160 and-or diastolic BP ≥ 100 despite three meds including a diuretic; and (3) rapidly declining kidney function with GFR slope < -3 over last yearProgression free survival from cardiovascular events, end stage renal disease, and these two combined with death was lower in in high-risk patients after stenting than after medical therapy alone. There was no difference in non-high-risk pts. This was driven by patients within the high-risk group who had RDKF (defined as a GFR slope < -3 mL/minute per year over last year. This was the 25th percentile of all patients pre-stenting). They also found that bilateral severe (> 70%). RAS was associated with increased risk for CVE, end stage renal disease, and both combined with death. Proteinuria < 1 g/day was associated with decreased risk of these
Li et al[26], 2026 (FAIR trial)Single center, prospective; 101 patients75.7% ± 14.3%Median = 138/80, IQR = 125-146/74-89GFR: Median = 55.8, IQR = 39.2-72.0Home SBP ≥ 140 and/or DBP ≥ 90 as well as ≥ 50% angiographic stenosisPatients were randomized to either an angiography guided group wherein all patients were stented, or a fractional flow reserve guided group wherein they were only stented if their FFR was < 0.8. Both groups had significantly reduced mean daily ambulatory SBP but required the same number of anti-hypertensives. When all stented patients with FFR < 0.8 were compared to stented patients with FFR > 0.8 and non-stented patients with FFR > 0.8 the mean daily ambulatory SBP was reduced in pts with FFR < 0.8 and these patients required fewer anti-hypertensive medications. FFR and percent stenosis angiographically were related logarithmically. FFR was measured using a dopamine induced gradient across the renal artery lesion
Iwashima et al[36], 2018Single center, retrospective; 139 patients60% of patients with severe (> 90% stenosis)154 ± 25/78 ± 14GFR: Mean = 45.2, SD = 20SBP > 140 and/or diastolic > 90 or receiving antihypertensive treatment and stenosis > 50% on angiography along with uncontrolled HTN, declining kidney function, or cardiac destabilization syndromePatients were categorized by GFR, UACR or UPCR and assessed for their risk of meeting a composite end point (defined as all-cause death, myocardial infarction, stroke, adverse aortic events, or end-stage renal failure requiring regular hemodialysis). Normal to mild risk group: UACR < 3, UPCR < 15, GFR > 45. Moderate risk group: UACR = 3-30, UPCR = 15-50, GFR = 30-44. Severe risk group: UACR > 30, UPCR > 50, GFR < 30. GFR < 30 and severe UACR/UPCR independently predicted higher likelihood of meeting primary composite endpoint
Meredith et al[38], 2017Single center retrospective; case-control; 188 patientsSurvivors: 79% ± 10%; non-survivors: 82% ± 10%Survivors: 156 ± 24/69 ± 13; non-survivors: 154 ± 28/68 ± 13Survivors GFR: Mean = 79, SD = 73; non-survivors GFR: Mean = 59, SD = 29≥ 70% atherosclerotic stenosis on concurrent coronary and renal angiographyPatients were split into survivors and non-survivors, and pre-stenting variables were compared between these two groups. Important predictors were identified using univariable regression and then included to a logistic regression. Previous MI, left ventricular ejection fraction < 35%, and GFR < 45 were predictors of mortality in a population of patients with renal artery stenosis > 70%. A survival benefit after RASt was seen in patients with 0 or 1 of these predictors but not 2 or 3 when compared to patients who were not stented. SBP, DBP, and stenosis severity were not correlated with survival
Koksal Cevher et al[21], 2026Single center, retrospective; 69 patientsLeft kidney: 85.5%; right kidney: 85.9%169.8 ± 29.8/96.8 ± 16.6Mean = 45.06, SD = 23.03> 60% stenosis with either resistant HTN, acute kidney injury, or flash pulmonary edemaAt one month follow up after stenting patients had lower SBP and DBP and required fewer antihypertensive medications, 55% of patients with acute kidney injury returned to baseline kidney function and 50% of patients with CKD exacerbations returned to baseline kidney function. Pulmonary edema resolved in all 16 patients it was found in at time of stenting
de Bhailis et al[19], 2024Single center, retrospective; 127 patientsMedian = 90%; IQR = 70%-95%Median = 160/77, IQR = 139-181/66.5-99.5Median = 40, IQR = 33.5-56> 50% stenosis of at least one artery and uncontrolled hypertension, deteriorating kidney function, or heart failure syndromeOf 127 patients were included in multidisciplinary discussions, 70 received medical therapy alone and 57 patients were stented (17 for HTN, 25 for deteriorating kidney function, 6 for heart failure syndromes, and 9 for severe anatomical stenosis); 82% of HTN patients experienced an improvement, 72% of deteriorating kidney function patients saw an attenuated GFR decline. All heart failure syndrome patients had no further heart failure admissions; 78% of anatomically severe stenosis patients had improved HTN and 55% had improved renal function. Additionally, patients who received stenting had more severe renal artery stenosis and more of them were on 3 or more anti-hypertensives prior to stenting compared to those who received medical treatment
Sens et al[18], 2019Single center, retrospective; 49 patientsN/AStent group: 150 ± 31/85 ± 17; medical group: 142 ± 27/76 ± 15Stent group GFR: Mean = 43, SD = 30; medical group GFR: Mean= 47, SD = 28Atherosclerotic renal artery stenosis with peak systolic velocity > 180 cm/second on duplex ultrasoundPatients who were stented had lower SBP and DBP with fewer required anti-hypertensive medications and unchanged GFR at one-year post-stenting. Medical therapy patients had no changes in these parameters. Of note, the baseline DBP was higher in the stent group, and this was a small sample size (n = 23 in stent group and n = 26 in medical therapy group)
Herrmann et al[31], 2016Single center, retrospective; 62 patientsStenosis > 60% (stent group only)Essential HTN group: 135 ± 19/71 ± 12; stent group: 143 ± 21/69 ± 7; medical group: 133 ± 19/67 ± 8Essential HTN group GFR: Mean = 77, SD = 20; stent group GFR: Mean = 53, SD = 20; medical group GFR: Mean = 63.6, SD = 21.3Non-diabetic white patients with renal artery stenosis > 60% compared to patients either with essential HTN or renal artery stenosis treated medically; 8 patients with bilateral high-grade stenosis excludedAfter stenting the GFR of the previously stenotic kidney rose and had reduced biomarkers of hypoxia. However, the contralateral kidney experienced a drop in GFR. Overall, there was no change in GFR after stenting. These results must be interpreted with caution due to small sample sizes and many pre-stenting differences between groups. Particularly the differences in GFR prior to stenting
Ma et al[29], 2016Meta-analysis of 7 studies; 253 patientsN/AN/AN/APatients with a single functioning kidneyMeta analysis of 7 papers including a total of 253 patients with single functioning kidneys, 77% of patients experienced improved or stabilized GFR after stenting. However, this should be interpreted with caution because the paper lacks significant detail about the other clinical and demographic information of these patients
Takahashi et al[37], 2020Single center, retrospective; 398 patientsN/AN/AGFR: Mean = 42.5, SD = 17.8All patients with data at pre-defined time points398 patients who had GFR measured 6-12 months before stenting, immediately prior to stenting, and 6-12 months after stenting. Lower GFR post-intervention, diabetes, higher proteinuria (grouped per 100 g per day), and CKD stages 4 and 5 were associated with higher likelihood of renal replacement and all-cause mortality after stenting


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