Renal function impairment is a frequent complication of endovascular aneurysm repair (EVAR), occurring in as many as 30% of patients. Although most patients recover, progression to advanced stages of chronic kidney disease (CKD) is associated with lower long-term survival.1 The risk of procedure-related acute kidney injury (AKI) can be mitigated by pre- and postoperative strategies and proper endovascular techniques. This article summarizes the factors affecting loss of renal function and strategies to optimize renal outcomes in patients undergoing EVAR.


Fenestrated or branched endovascular aneurysm repair (F/BEVAR) using custom-made or patient-specific devices provides the best long-term results with respect to target vessel outcomes. Although it is logical to assume that F/BEVAR carries higher risk of renal injury compared with standard EVAR, de Souza et al have shown nearly identical outcomes with both types of repair.1 A decline in renal function occurred in 27% of patients after FEVAR and in 42% of patients after EVAR at 5 years (P = .5). Tran and colleagues also reported on renal function outcomes among 110 FEVAR patients.2 Freedom from renal function deterioration occurred in 62% of patients at 2 years, which is somewhat lower than what was reported by our group (74% at 3 years).2,3 These differences are most likely explained by how investigators define deterioration. Tran et al defined deterioration as any change to a worse CKD category, whereas our study used > 25% decline in baseline estimated glomerular filtration rate (eGFR).2,3 Results with parallel grafts were reported by the Stanford group, including progression in CKD stage in 41% of patients and 76% freedom from renal function deterioration at 1 year.4 For open repair, Mills and colleagues reported an 18% to 39% rate of renal function deterioration at 2 years.5


Multiple mechanisms explain the acute and late insult in renal function after complex endovascular repair. Among patients who develop AKI, persistence of a silent inflammatory response may trigger fibrotic changes in the renal parenchyma, leading to long-term structural and functional damage.6 The main pathologic change associated with AKI is tubulointerstitial fibrosis (TIF), sparing the glomeruli. The fibrotic process occurs as lethally injured cells heal or as sublethally injured cells recover. The degree of TIF correlates with progression of CKD even after the acute phase and initial recovery.7 It is likely that the persistence of pathologic processes that initiated the AKI (eg, inflammation, hypoxia, cellular senescence, maladaptive repair) leads to CKD progression through self-perpetuating TIF.8 We have found that patients who developed AKI after F/BEVAR had a fourfold increased risk of renal function deterioration.3 Another proposed mechanism is that systemic hypertension causes progression of kidney fibrosis. Picken and colleagues have described the association of renal parenchyma loss leading to glomerular hypertension, impaired kidney blood flow autoregulation, hyperfiltration, hypertrophy, and, ultimately, barotrauma-mediated glomerulosclerosis-induced TIF.9

Atheroembolism is also a cause of AKI, presumably due to ischemia, although cholesterol crystals lodged in the microvasculature can be a direct source of acute and chronic inflammatory changes that result in encasement by histiocytes, intimal proliferation, and fibrosis.10 Contrast-induced nephrotoxicity may perpetuate this vicious circle of medullary ischemia and TIF.11

Renal function reserve (RFR) is described as the kidneys’ capacity to maintain adequate filtration after significant loss of cells.12 Some patients, particularly the elderly, may have significant renal impairment despite a normal baseline eGFR because of decreased RFR. The microanatomic structural changes of the kidney with older age include a decreased number of functional glomeruli from an increased prevalence of nephrosclerosis (arteriosclerosis, glomerulosclerosis, tubular atrophy with interstitial fibrosis) and, to some extent, compensatory hypertrophy of remaining nephrons.13 Patients with limited preoperative RFR cannot recover after AKI and have continued decline of renal function. Conversely, patients with normal RFR may recover from AKI and maintain normal eGFR despite the permanent reductions in RFR. These patients are therefore more susceptible to subsequent changes in renal function with recurrent insults.14


Historically, the definition of renal injury has widely varied in the literature, leading to discrepancy between reports.15 Some studies focused on change in serum creatinine or need for renal replacement therapy, which underestimates the incidence of AKI.16 The Acute Dialysis Quality Initiative group introduced the risk, injury, failure, loss, and end-stage (RIFLE) classification based on serum creatinine concentration, eGFR, and urine output measurements.17,18 These consensus criteria were the first to recognize less severe stages of AKI (Table 1).

Cystatin C is a plasma protein that is produced by nucleated human cells and is a more sensitive marker of renal injury than serum creatinine and GFR. Its use is rarely applied in clinical practice.19 Evaluation of cystatin C after EVAR has shown contradicting results, with some reports showing no impact and others showing significant deterioration.20,21


AKI likely occurs due to systemic factors, ischemia, contrast-induced nephropathy, atheroembolism, renal artery ostial disease, renal artery trauma, and inflammatory reaction (Figure 1). A single-center report detailed a comparison between open repair and FEVAR.22 FEVAR demonstrated an advantage, with only 9% versus 27% new-onset renal insufficiency and 3% requiring dialysis in both groups; however, this difference did not persist. During the 2-year follow-up, there was a small increase in new-onset renal insufficiency in both groups (12% vs 6%) without statistical difference. Similarly, a systematic review demonstrated a minimal difference in renal insufficiency between open repair and FEVAR (14% vs 11%, respectively).23

Figure 1. Contributing factors to AKI during complex endovascular procedures. Reprinted with permission from Mayo Foundation for Medical Education and Research.

Preoperative Measures

Detailed preoperative and intraoperative imaging implies the need to administer nephrotoxic contrast agents. Patients with normal or mildly elevated creatinine (< 1.8 mg/dL) can withstand a standard CT scan in conjunction with hydration with minimal risks. In patients with GFR < 44 mL/min/1.73 m2 (stage 3B CKD), we have used a low-iodine CTA protocol (Table 2).24 This has replaced the use of catheter-directed CT scans.

Data suggest that preoperative hydration with either saline or sodium bicarbonate reduces the risks associated with nephrotoxic agents administered during contrast interventions, with no advantage of either fluid over the other.25 In patients with normal renal function, the impact of prehydration is less dramatic. However, in patients with preexisting chronic renal insufficiency, prehydration has been shown to be beneficial.26 The use of N-acetylcysteine is controversial, with some studies suggesting benefit and other reports showing no added benefit.27-29 Multiantioxidant supplementation demonstrated a brief period of higher creatinine clearance but had no impact on serum creatinine after open abdominal aortic aneurysm (AAA) repair.30 Mannitol administered during open AAA repair has been demonstrated to reduce subclinical renal injury and showed a small benefit in patients undergoing EVAR when administered with hydration in a randomized trial.31,32 However, in a much larger review, mannitol was not beneficial in the open repair setting.33

Patients who take metformin, a common oral hypoglycemic agent, need special consideration when also receiving intravenous contrast. Metformin is excreted by the kidneys, and impaired clearance in the setting of renal dysfunction results in lactic acidosis. Low-osmolality contrast agents should be used in this scenario. A number of oral hypoglycemic agents contain metformin in combination with other medications, and attention to these medications is warranted. Holding metformin either before or after the angiographic procedure should be strongly considered.

Figure 2. AWT volume measurement sequence. Step 1: Total segmental volume measurement. Step 2: Luminal volume subtraction. Step 3: Remaining residual volume corresponding to the aortic wall and thrombus volume. Reprinted with permission from Mayo Foundation for Medical Education and Research.

The volume of aortic wall thrombus (AWT) can predict risk of embolization during endovascular procedures. Ribeiro et al assessed the volume of AWT by calculating an index (Figure 2), which was representative of the solid portion of the aortic wall after excluding the blood volume.34 In addition, a qualitative analysis of AWT was performed using the number of aortic segments involved, thrombus type, thrombus thickness, thrombus area, and thrombus circumference (Figure 3). The most severely affected segment of the aorta was considered to characterize the thrombus (Figure 4). Using this grading system, patients with severe thrombus had higher rates of AKI and greater decline in eGFR in the first month after the operation. Kidney infarcts were present in 31% of patients with severe thrombus compared with 11% of those with mild AWT. Also, severe thrombus was an important determinant of renal function deterioration.3,34

Figure 3. Qualitative score-based classification of AWT. The most severely affected aortic area in the CTA cross-section is classified for thrombus type (none, smooth lining, or finger-like projections), thickness (none, 1–4 mm, or > 5 mm), area (0%–24%, 25%–50%, or > 50%), and circumference (0–90°, 91–179°, or > 180°). Number of affected segments is also considered. Individual items are graded from 0 to 2. Mild AWT ranges from 0 to 4, moderate AWT from 4 to 8, and severe AWT scores 9 and 10. Image reproduced by permission of Mayo Foundation for Medical Education and Research.

Figure 4. Axial and sagittal CTA sections exemplify the three AWT graduations by the proposed classification. Mild AWT patients have very slight and regular atheroma plaques without diffuse disease. Moderate AWT patients usually have higher amount of debris, with or without finger-like thrombus, whereas severe AWT patients have extremely irregular, large, and diffuse thrombus. Reprinted with permission from Mayo Foundation for Medical Education and Research.

Intraoperative Measures

Meticulous implantation technique is essential to minimize the risk of renal injury. Because of the complexity of these repairs, multiple steps can be associated with deleterious effects to the kidney. Misalignment of fenestrations or an occlusive renal sheath can prolong renal ischemia. Embolization due to large or microscopic debris can occur during device orientation, deployment, and branch vessel stenting. Because these devices require larger-profile systems, using a filter is not a practical alternative. Excessive use of contrast media can be associated with added risk of nephrotoxicity. Finally, selective catheterization and stenting of the renal target should be performed with meticulous technique to avoid inadvertent perforation or dissection.

There is no substitute for meticulous procedural technique to avoid renal complications associated with F/BEVAR. Careful attention to the position of the renal wires as well as identifying potential side branch positions and accurate stent placement is critical in avoiding renal complications. Excessive manipulations, especially in the presence of orificial renal disease, can result in atheroembolic events. Branched devices may require more intra-aortic manipulation compared with fenestrated devices. Renal complications appear to be more common earlier in practitioners’ experience in reported series.35 The procedure should be planned with the goal of limiting catheter manipulations. For example, ptotic renal arteries may be best approached from the upper extremities or using a steerable sheath. During the procedure, additional time should be spent positioning and flaring the renal stents. Obtaining orthogonal views to the fenestration and placing the stent approximately 5 mm into the aortic endoprosthesis allows for sufficient overlap and flaring. Compression and occlusion of target stents can occur with insertion or removal of additional stent graft components. If suspected, protecting the stent with a balloon during device manipulation is helpful. Three-dimensional rotational angiography and cone-beam CT can help identify these defects prior to leaving the operating room.

Inaccurate device positioning can result in excessive device manipulation, leading to atheroemboli and longer operations. Lower extremity ischemia from large sheaths is associated with morbidity and mortality after F/BEVAR.36 Close monitoring of urine output postoperatively as well as hydration and bicarbonate administration may help prevent renal injury from elevated levels of creatine kinase. Lastly, reducing contrast administration during the procedure can be beneficial in decreasing the incidence of contrast-induced nephropathy. Injections of half- and one-third–strength contrast dilution can help minimize the contrast load. Similarly, using onlay fusion can assist in minimizing contrast. Intravascular ultrasound has also been used to facilitate alignment of the graft and, in combination with fusion imaging, may help reduce extra manipulations caused from precannulation. Although gadolinium and carbon dioxide have been used to reduce the risks associated with contrast angiography, these do not come without inherent risks as well. Gadolinium can cause nephrogenic systemic fibrosis in patients with severe preexisting renal dysfunction,37 and carbon dioxide may lead to gas embolism above the diaphragmatic level.

Postoperative Measures

Patients should be closely monitored postoperatively to avoid hypotension and hypovolemia. Duplex ultrasound may help determine patency of renal targets. Renal parenchymal perforation and perinephric hematoma should be suspected in patients with a reduction in hemoglobin or severe flank pain. Close surveillance of renal stents by duplex ultrasound is undertaken approximately every 6 months during the first year and yearly thereafter.


Complex endovascular aortic repair is associated with a 20% to 30% risk of AKI, but dialysis is needed in only 1% to 3% of patients treated at high-volume centers. Meticulous preoperative planning with appropriate hydration can help reduce these risks, especially in patients with preexisting renal insufficiency. During the procedure, the use of advanced imaging techniques along with limited manipulations, judicious intravenous contrast administration, and careful protection of the stents during device implantation help minimize the risk of injury. Patients require routine follow-up to detect renal complications during the postoperative period, with 40% of patients recovering after acute renal insult to within 30% of their baseline function.

1. de Souza LR, Oderich GS, Farber MA, et al. Comparison of renal outcomes in patients treated by Zenith® fenestrated and Zenith® abdominal aortic aneurysm stent grafts in US prospective pivotal trials. Eur J Vasc Endovasc Surg. 2017;53:648-655.

2. Tran K, Fajardo A, Ullery BW, et al. Renal function changes after fenestrated endovascular aneurysm repair. J Vasc Surg. 2016;64:273-280.

3. Sandri GA, Oderich GS, Tenorio ER, et al. Impact of aortic wall thrombus on late changes in renal function among patients treated by fenestrated-branched endografts. J Vasc Surg. 2019;69:651-660.e4.

4. Lee JT, Varu VN, Tran K, Dalman RL. Renal function changes after snorkel/chimney repair of juxtarenal aneurysms. J Vasc Surg. 2014;60:563-570.

5. Mills JL Sr, Duong ST, Leon LR Jr, et al. Comparison of the effects of open and endovascular aortic aneurysm repair on long-term renal function using chronic kidney disease staging based on glomerular filtration rate. J Vasc Surg. 2008;47:1141-1149.

6. van Kuijk JP, Flu WJ, Chonchol M, et al. Temporary perioperative decline of renal function is an independent predictor for chronic kidney disease. Clin J Am Soc Nephrol. 2010;5:1198-1204.

7. Hodgkins KS, Schnaper HW. Tubulointerstitial injury and the progression of chronic kidney disease. Pediatr Nephrol. 2012;27:901-909.

8. Go AS, Chertow GM, Fan D, et al. Chronic kidney disease and the risks of death, cardiovascular events, and hospitalization. N Engl J Med. 2004;351:1296-1305.

9. Picken M, Long J, Williamson GA, Polichnowski AJ. Progression of chronic kidney disease after acute kidney injury: role of self-perpetuating vs. hemodynamic-induced fibrosis. Hypertension. 2016;68:921-928.

10. Mulay SR, Evan A, Anders HJ. Molecular mechanisms of crystal-related kidney inflammation and injury. Implications for cholesterol embolism, crystalline nephropathies and kidney stone disease. Nephrol Dial Transplant. 2013;29:507-514.

11. Merten GJ, Burgess WP, Gray LV, et al. Prevention of contrast-induced nephropathy with sodium bicarbonate: a randomized controlled trial. JAMA. 2004;291:2328-2334.

12. Denic A, Glassock RJ, Rule AD. Structural and functional changes with the aging kidney. Adv Chronic Kidney Dis. 2016;23:19-28.

13. Bosch JP, Saccaggi A, Lauer A, et al. Renal functional reserve in humans: effect of protein intake on glomerular filtration rate. Am J Med. 1983;75:943-950.

14. Ronco C, Rosner MH. Acute kidney injury and residual renal function. Crit Care. 2012;16:144.

15. Hoste EA, Kellum JA. Incidence, classification, and outcomes of acute kidney injury. Contrib Nephrol. 2007;156:32-38.

16. Bihorac A, Brennan M, Ozrazgat-Baslanti T, et al. National surgical quality improvement program underestimates the risk associated with mild and moderate postoperative acute kidney injury. Crit Care Med. 2013;41:2570-2583.

17. Bellomo R, Ronco C, Kellum JA, et al. Acute renal failure—definition, outcome measures, animal models, fluid therapy and information technology needs: the second International Consensus Conference of the Acute Dialysis Quality Initiative (ADQI) group. Crit Care. 2004;8:R204-R212.

18. Kellum JA, Lameire N, Aspelin P, et al. KDIGO clinical practice guideline for acute kidney injury. Kidney Int. 2012;2(suppl):1-141.

19. Deinum J, Derkx FH. Cystatin for estimation of glomerular filtration rate? Lancet. 2000;356:1624-1625.

20. Davey P, Peaston R, Rose JD, et al. Impact on renal function after endovascular aneurysm repair with uncovered supra-renal fixation assessed by serum cystatin C. Eur J Vasc Endovasc Surg. 2008;35:439-445.

21. Abdelhamid MF, Davies RS, Vohra RK, et al. Assessment of renal function by means of cystatin C following standard and fenestrated endovascular aneurysm repair. Ann Vasc Surg. 2013;27:708-713.

22. Shahverdyan R, Majd M, Thul R, et al. F-EVAR does not impair renal function more than open surgery for juxtarenal aortic aneurysms: single centre results. Eur J Vasc Endovasc Surg. 2015;50:432-441.

23. Rao R, Lane TR, Franklin IJ, Davies AH. Open repair versus fenestrated endovascular aneurysm repair of juxtarenal aneurysms. J Vasc Surg. 2015;61:242-255.e5.

24. Vasconcelos R, Vrtiska TJ, Foley TA, et al. Reducing iodine contrast volume in CT angiography of the abdominal aorta using integrated tube potential selection and weight-based method without compromising image quality. AJR Am J Roentgenol. 2017;208:552-563.

25. Hogan SE, L’Allier P, Chetcuti S, et al. Current role of sodium bicarbonate-based preprocedural hydration for the prevention of contrast-induced acute kidney injury: a meta-analysis. Am Heart J. 2008;156:414-421.

26. Taylor AJ, Hotchkiss D, Morse RW, McCabe J. PREPARED: preparation for angiography in renal dysfunction: a randomized trial of inpatient vs outpatient hydration protocols for cardiac catheterization in mild-to-moderate renal dysfunction. Chest. 1998;114:1570-1574.

27. Kelly AM, Dwamena B, Cronin P, et al. Meta-analysis: effectiveness of drugs for preventing contrast-induced nephropathy. Ann Intern Med. 2008;148:284-294.

28. Lawlor DK, Moist L, DeRose G, et al. Prevention of contrast-induced nephropathy in vascular surgery patients. Ann Vasc Surg. 2007;21:593-597.

29. Moore NN, Lapsley M, Norden AG, et al. Does N-acetylcysteine prevent contrast-induced nephropathy during endovascular AAA repair? A randomized controlled pilot study. J Endovasc Ther. 2006;13:660-666.

30. Wijnen M, Vader H, Van Den Wall Bake AW, Roumen R. Can renal dysfunction after infra-renal aortic aneurysm repair be modified by multi-antioxidant supplementation? J Cardiovasc Surg (Torino). 2002;43:483-488.

31. Nicholson ML, Baker DM, Hopkinson BR, Wenham PW. Randomized controlled trial of the effect of mannitol on renal reperfusion injury during aortic aneurysm surgery. Br J Surg. 1996;83:1230-1233.

32. Kalimeris K, Nikolakopoulos N, Riga M, Christodoulaki K, et al. Mannitol and renal dysfunction after endovascular aortic aneurysm repair procedures: a randomized trial. J Cardiothorac Vasc Anesth. 2014;28:954-959.

33. Hersey P, Poullis M. Does the administration of mannitol prevent renal failure in open abdominal aortic aneurysm surgery? Interact Cardiovasc Thorac Surg. 2008;7:906-909.

34. Ribeiro M, Oderich GS, Macedo T, et al. Assessment of aortic wall thrombus predicts outcomes of endovascular repair of complex aortic aneurysms using fenestrated and branched endografts. J Vasc Surg. 2017;66:1321-1333.

35. Haddad F, Greenberg RK, Walker E, et al. Fenestrated endovascular grafting: the renal side of the story. J Vasc Surg. 2005;41:181-190.

36. Miller CC III, Grimm JC, Estrera AL, et al. Postoperative renal function preservation with nonischemic femoral arterial cannulation for thoracoabdominal aortic repair. J Vasc Surg. 2010;51:38-42.

37. Khawaja AZ, Cassidy DB, Al Shakarchi J, et al. Revisiting the risks of MRI with gadolinium based contrast agents—review of literature and guidelines. Insights Imaging. 2015;6:553-558.

Gustavo S. Oderich, MD
Chair, Division of Vascular and Endovascular Surgery
Professor of Surgery
Program Director, Vascular and Endovascular Surgery Integrated Residency and Fellowship
Program Director, Advanced Endovascular Aortic Fellowship
Mayo Clinic
Rochester, Minnesota
Disclosures: Consulting fees and grants from Cook Medical, Gore & Associates, and GE Healthcare (all paid to Mayo Clinic; no personal income).

Emanuel R. Tenorio, MD, PhD
Aortic Research Fellow
Division of Vascular and Endovascular Surgery
Mayo Clinic
Rochester, Minnesota
Disclosures: None.