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Impact and Predictors of Acute Kidney Injury After Endovascular Aneurysm Repair
Benjamin R Zambetti, William P Zickler, Saskya Byerly, H Edward Garrett, Jr., Louis J Magnotti
University of Tennessee Health Science Center, Memphis, TN

Introduction: Acute kidney injury (AKI) after endovascular aneurysm repair (EVAR) is uncommon though carries significant morbidity. Multiple studies have shown that post-operative AKI increases length of stay (LOS), morbidity, and mortality, though pre-operative and procedural risk factors are not well established. The goal of this study was to examine the impact of AKI on patients undergoing EVAR and identify risk factors for AKI using a large, national dataset.
Methods: Patients undergoing EVAR were identified from the National Surgical Quality Improvement Program (NSQIP) database over 9 years, ending in 2019. Patients on dialysis were excluded. Age, gender, race, indication for repair (size, rupture, symptomatic, dissection), proximal and distal landing zones, comorbidities (diabetes, tobacco use, COPD, CHF, CKD), pre-operative transfusion requirements, procedural details (ASA class, aortic diameter, operative time, wound classification, elective repair), complications (AKI, pneumonia, failure to wean from the ventilator, PE, DVT, post-operative sepsis), hospital LOS, ICU LOS and mortality were recorded. Patients were then stratified by presence of AKI and compared. Multivariable logistic regression (MLR) analysis was performed to determine independent predictors of AKI.
Results: 18347 patients were identified. The majority were male (81%), white (78%), with a median age and aortic diameter of 74 and 5.5, respectively and had undergone an elective repair (78%). The median operative time was 120 minutes. Of these 234 (1.3%) developed AKI. Patients who developed AKI were more often male (81 vs 70%, p<0.0001), had larger aortic diameters (6.6 vs 5.5cm, p<0.0001), higher pre-operative creatinine (1.6 vs 1.0, p<0.0001), lower hematocrit (35 vs 41, p<0.0001), were more often juxta-renal (17 vs 5%, p<0.0001), required more pre-operative transfusions (21 vs 2%, p<0.0001), and were more often for rupture (49 vs 7%, p<0.0001). Postoperative complications were all more common in patients who developed AKI (Table 1). Mortality (40 vs 1.8%, p<0.0001), ICU LOS (5 vs 0 days, p<0.0001), and hospital LOS (11 vs 2 days, p<0.0001) were all significantly increased in patients with AKI. After adjusting for demographics, pre-operative and procedural factors, MLR identified increasing diameter, creatinine, operative time, preoperative transfusions, ASA class, and juxtarenal/suprarenal proximal landing zone as predictors of AKI (Table 2). Only elective repair and male sex were found to be protective against AKI (Table 2).
Conclusions: AKI after EVAR causes significant morbidity, prolonged hospitalizations, and increases mortality rates. In fact, patients who developed AKI were 20 times more likely to die within 30-days of surgery. MLR failed to identify any modifiable risk factors protective against AKI in patients undergoing EVAR. Thus, those patients at risk of AKI after EVAR should be closely monitored to reduce both morbidity and mortality.
Table 1:

Total, n18113234
Pneumonia240 (1.3)55 (23.5)<0.0001
Pulmonary embolism44 (0.2)3 (1.3)0.022
Ventilator >48hrs252 (1.4)116 (49.6)<0.0001
UTI229 (1.3)7 (3)0.032
CVA69 (0.4)8 (3.4)<0.0001
Cardiac Arrest185 (1)33 (14.1)<0.0001
MI275 (1.5)35 (15)<0.0001
DVT86 (0.5)9 (3.9)<0.0001
Sepsis120 (0.7)11 (4.7)<0.0001
Intra/Post-Operative Transfusion2155 (11.9)167 (71.4)<0.0001
Return OR849 (4.7)88 (37.7)<0.0001

Table 2:
Odds Ratio95% Confidence Intervalp
OR Time1.0061.005-1.007<0.0001
Preop Transfusion3.0221.938-4.714<0.0001

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