The incidence of acute kidney injury (AKI) after major abdominal surgery ranges from 3.5%1 to 13.4%2 and is associated with morbidity and mortality.2,3 Although the mechanisms underlying the development of AKI are multifactorial,4,5 the toxic effects of the perioperative inflammatory response may play an important role.6–8 Although the inflammatory responses induced by surgery are important for maintaining postoperative homeostasis, severe dysregulation of the inflammatory process, such as complement and leukocytic cell activation producing inflammatory cytokines, may predispose to end-organ complications such as AKI.8,9
Propofol and sevoflurane, widely used general anesthetics, have been shown to modulate the inflammatory responses to surgical stimulations in both clinical and experimental studies.7,10–12 Previous reports have demonstrated that propofol reduces the lipopolysaccharide proinflammatory cytokine response and improves cell survival in an in vitro neuroinflammatory model.13 Sevoflurane, another anesthetic with anti-inflammatory action,14 suppresses local alveolar inflammatory response in patients undergoing thoracic surgery.10
The effects of propofol and sevoflurane on postoperative AKI are incompletely understood. In animal models of renal ischemia–reperfusion (IR), propofol reduces oxidative stress,11 and in a 2014 clinical study of AKI after cardiac surgery, propofol exerted a protective effect relative to sevoflurane.12 The effect of sevoflurane on renal function is less clear. In rat models, sevoflurane decreased AKI and reduced inflammatory responses during liver transplantation.15 However, older studies link sevoflurane to increased perioperative renal toxicity.10,11,16,17 It is not clear which anesthetic more effectively prevents postoperative AKI after major abdominal surgery.
The aim of the present study was to compare the incidence of AKI diagnosed by Acute Kidney Injury Network (AKIN) and risk, injury, failure, loss, and end-stage renal disease (RIFLE) criteria after colorectal surgery in patients anesthetized with propofol or sevoflurane and to identify the predictors of AKI in our patient population. We also evaluated the impact of AKI on short-term and long-term morbidity and mortality.
We reviewed the electronic medical records and laboratory results of all patients who underwent colorectal surgery in Asan Medical Center between January 2008 and December 2011. A total of 4958 consecutive adult patients who had undergone colorectal surgeries were identified through our electrical medical recording system. Of these, 638 were excluded, including 39 patients with repeated operations, 96 patients with combined operations on parts other than large or small bowel, 11 patients anesthetized with anesthetics other than sevoflurane or propofol (1 with desflurane, 1 with isoflurane, and 9 with regional anesthesia), and 492 patients for whom preoperative or postoperative serum creatinine (sCr) values were not available. Thus, 4320 patients were included in the final analysis. Patients were divided into 2 groups according to the anesthetic type (propofol group: n = 3055 and the sevoflurane group: n = 1265). Both groups of patients received remifentanil as the primary intraoperative opioid. The study protocol was approved by the IRB of our institution (2012–0132), which waived the requirement for informed consent because of the retrospective design of the analysis.
The computerized patient record system of our institution (Asan Medical Center Information System Electronic Medical Records) was reviewed retrospectively to obtain demographic, laboratory, surgical, and anesthetic data on all patients and their postoperative outcomes. Demographic data included patient age, sex, body mass index (BMI), smoking history, comorbidities (hypertension [HTN], diabetes mellitus [DM], ischemic heart disease, chronic obstructive pulmonary disease, cerebrovascular accident, and chronic kidney disease), and use of prescribed medications (calcium channel blockers, angiotensin-converting enzyme inhibitors/angiotensin receptor blockers, β-blockers, aspirin, antiplatelet agents, oral hypoglycemic agents, and 3-hydroxy-3-methylglutaryl-coenzyme A reductase inhibitor). HTN was defined as the use of any antihypertensive medications at admission, DM as the use of any hypoglycemic agents, ischemic heart disease as positive coronary angiography or compatible electrocardiographic or perfusion scan findings, cerebrovascular accident as positive magnetic resonance imaging findings or neurologic sequelae, and chronic kidney disease as a baseline estimated glomerular filtration rate (eGFR) <60 mL/min/1.73 m2. Chronic obstructive pulmonary disease was documented by certified pulmonologists.
Laboratory data included hemoglobin, sCr, albumin, serum uric acid, and eGFR. Serum albumin concentrations at baseline were measured by the use of the bromocresol green dye-binding method.18 eGFR was estimated from the preoperative sCr concentration with the Modification of Diet in Renal Disease study equation for adult patients and adjusted for each 1.73 m2 of body surface area.19 Surgical and anesthetic data included the type of surgical procedure (laparoscope or open), urgency of the operation, volume and type of fluids (crystalloid and colloid), volume of packed red blood cells, duration of anesthesia, lowest intraoperative mean blood pressure, anesthetic agents (sevoflurane and propofol), and the intraoperative use of furosemide. Colloid agents used during surgery included 10% hydroxyl ethyl starch 260/0.45 (Pentaspan™; Bristol-Myers Squibb, Montreal, Canada), 6% hydroxyl ethyl starch 130/0.4 (Voluven®; Fresenius Kabi, Bad Homburg, Germany), and albumin.
Definition of Outcomes
Outcome variables included postoperative AKI, postoperative intensive care unit (ICU) admission, 30-day major adverse cardiovascular events (MACE), 30-day mortality, and overall survival. Postoperative AKI was diagnosed by AKIN and RIFLE criteria via the alteration of the sCr concentration on postoperative 1 to 7 days compared with the baseline sCr concentration defined as the last concentration measured before surgery. If sCr was measured more than once per day within postoperative 7 days, the highest reading of that day was used. MACE included cardiovascular complications, including myocardial infarction, atrial fibrillation with rapid ventricular response, new onset or aggravating heart failure, and recurrent stroke, which occurred postoperatively.20 In-hospital mortality was determined by review of electrical medical records. For validation of complete follow-up data regarding mortality, information about the date of death was obtained from the National Population Registry of the Korea National Statistical Office using a unique personal identification number for each patient.
Continuous variables were reported as mean ± SD or median and interquartile range (IQR). All continuous data were evaluated for normality using the Shapiro-Wilk test, and parametric and nonparametric tests were applied when appropriate for inferential statistics. Patient age, height, weight, BMI, laboratory data, amounts of administered packed red blood cells and fluids, urine output, lowest intraoperative mean blood pressure, and duration of anesthesia were compared with the Student t test. Categorical variables are expressed as frequencies and percentages and analyzed with the χ2 test or the Fisher exact test, as appropriate. Multiple logistic regression analysis was performed to identify independent predictors of AKI and to evaluate the impact of anesthetic type on outcome variables. All variables with P < 0.1 on univariate analysis were included in the multivariable analysis. Discrimination of the model was assessed by C statistics, and calibration was evaluated with the Hosmer-Lemeshow statistics.
Weighted logistic regression and multivariate Cox’s proportional hazard regression were performed to assess the adjusted odds ratios (ORs) and hazard ratios for the effect of anesthetic type on outcome variables. The proportional-hazards assumption for each variable was checked by Schoenfeld residuals and the double-log method. To reduce the influence of confounding variables, propensity score (PS) matching method was used to adjust intergroup differences between sevoflurane and propofol group. We calculated the PS for each patient by modeling the probability of being anesthetized with propofol or sevoflurane. We subsequently used the derived PS values to match 1265 patients in the sevoflurane group with the patients in propofol group at a ratio of 1:1 using a greedy matching algorithm.21 All variables shown in Table 1 without regard to outcomes were used to obtain the PS. After all PS matches were performed, we assessed the balance in baseline covariates through paired t tests/McNemar tests and standardized mean difference as appropriate for continuous and categorical variables.
All P values <0.05 were considered statistically significant. Data manipulation and statistical analyses were done using SAS® version 9.1 (SAS Institute Inc, Cary, NC) or R software version 2.10.1.
A total of 4320 patients were included in the final analysis. The median follow-up for the overall patient population was 3.1 (IQR, 2.2–3.9) years. The baseline characteristics of patients according to the anesthetic type are summarized in Table 1. Laboratory variables did not differ between the 2 groups, except that the eGFR was greater in the sevoflurane group. Before propensity matching, patients in the sevoflurane group were more likely to undergo emergent surgery, require diuretics during the operation, and have laparoscopic surgery than patients in the propofol group (Table 1). The balance between matched patients is summarized in Table 2.
The demographic characteristics and the outcomes of patients who underwent emergent surgery are summarized in Supplementary Table S1 (Supplemental Digital Content, http://links.lww.com/AA/B405). The patients who underwent emergent surgery showed significantly greater ASA physical status, lower eGFR, serum albumin level, and lowest intraoperative mean blood pressure. In addition, they were anesthetized with sevoflurane more often, required more diuretics, fluid administration, and intraoperative pRBCs transfusion.
Overall, AKI occurred in 414 (9.6%) of patients using AKIN criteria. The prevalence of AKI was greater in the sevoflurane group (n = 142, 11.2%) than that in the propofol group (n = 272, 8.9%) (P = 0.02). When RIFLE criteria were used, AKI occurred in 251 patients (5.8%) overall. Again, the sevoflurane group had a greater incidence of AKI (n = 94, 7.4%) compared with the propofol group (n = 157, 5.1%) (P = 0.004). Multivariate analysis identified the following independent predictors of AKI: age (OR, 1.02; 95% confidence interval [CI], 1.01–1.03; P = 0.0078 by AKIN; OR, 1.01; 95% CI, 1.00–1.03; P = 0.01 by RIFLE), sevoflurane (OR, 1.29; 95% CI, 1.03–1.61; P = 0.03 by AKIN; OR, 1.44; 95% CI, 1.09–1.91; P = 0.02), emergent operation (OR, 1.89; 95% CI, 1.03–3.49; P = 0.04 by AKIN; OR, 3.52; 95% CI, 1.92–6.45; P = 0.0024 by RIFLE), diuretics (OR, 2.44; 95% CI, 1.15–5.17; P = 0.02 by AKIN; OR, 3.26; 95% CI, 1.45–7.30; P = 0.005 by RIFLE), preoperative albumin level (OR, 0.76; 95% CI, 0.63–0.92; P = 0.0042 by AKIN; OR, 0.74; 95% CI, 0.59–0.93; P = 0.0022 by RIFLE), and DM (OR, 1.53; 95% CI, 1.17–2.00; P = 0.0005 by AKIN; OR, 1.51; 95% CI, 1.08–2.11; P = 0.02 by RIFLE; Table 3; Supplemental Digital Content, Supplemental Table S3, http://links.lww.com/AA/B405). Moreover, HTN (by AKIN) and β-blocker (by RIFLE) were associated with AKI prediction.
Univariate and multivariate predictors of overall mortality are shown in Supplementary Table S2 (Supplemental Digital Content, http://links.lww.com/AA/B405). In multivariate analysis, BMI, ASA physical status, emergent operation, anesthetic time, and DM were associated with overall mortality. However, AKI was not associated with overall mortality. Patients who received sevoflurane had longer hospital stays (median [IQR], 7 [6–9] days) than those who received propofol (median [IQR], 7 [6–8] days) (P < 0.01) and higher ICU admission rates (6.4% vs 4.7%, P = 0.025).
The unadjusted (univariate analysis) effect of anesthetics on the incidence of outcome variables is shown in Figure 1. Mortality within 30 postoperative days was higher in the sevoflurane group than that in the propofol group (P = 0.01), but the incidence of MACE (P = 0.07) and overall mortality (P = 0.14) did not differ between the 2 groups. The incidence of AKI according to the diagnosis and type of operation is summarized in Table 4. Most patients were diagnosed with colorectal cancer (n = 3843, 90%). The remainder was diagnosed with the Crohn disease, benign lesion, ileus, or ischemia.
The association between sevoflurane and postoperative outcomes is shown in Tables 5 and 6. Before propensity matching was performed, multivariate-adjusted analysis identified sevoflurane as the only predictor of postoperative AKI by AKIN (OR, 1.29; 95% CI, 1.03–1.61; P = 0.03) and RIFLE (OR, 1.44; 95% CI, 1.09–1.91; P = 0.02) criteria. After PS matching (n = 1249 pairs), the association was considerably weaker. AKI defined by RIFLE criteria remained weakly correlated (OR, 1.41; 95% CI, 1.02–1.95; P = 0.04) with sevoflurane use but not AKI by AKIN criteria (P = 0.06). However, differences in ICU admission, 30-day mortality, and overall mortality did not differ between the 2 groups (P = 0.41, P = 0.18, and P = 0.68, each respectively).
In this retrospective study, we explored the relationship between anesthetic agent and postoperative outcomes in patients who underwent colorectal surgery. Overall, we found a lower incidence of AKI in the propofol group according to AKIN (5.1%) and RIFLE (7.4%) criteria compared with sevoflurane group (8.9% and 11.2%, respectively). Multivariate analysis revealed that sevoflurane was a risk factor of postoperative AKI by AKIN (P = 0.03) and RIFLE (P = 0.02) criteria. After propensity matching to adjust for potential confounding factors, sevoflurane may be associated with postoperative AKI when the RIFLE criteria are used (P = 0.04) and not associated with AKI when AKIN criteria are used. Patients presenting for emergent surgery were more likely to be anesthetized with sevoflurane, which was not associated with an increase in mortality or ICU admission.
Although postoperative AKI after cardiovascular surgery has been investigated extensively,22,23 only a few reports have discussed how AKI evolves after major noncardiac surgery.1,5,24 Known predictors of AKI include older age, male sex, hypoalbuminemia, active congestive heart failure, ascites, HTN, greater ASA physical status, emergency surgery, intraperitoneal surgery, renal insufficiency, and DM.4,5,25 Our multivariate analysis revealed similar risk factors, finding, in addition to sevoflurane versus propofol, that age, emergency operation, diuretics, preoperative albumin level, DM, HTN, and β-blockers were associated with AKI by AKIN and RIFLE criteria. To our knowledge, propofol and sevoflurane for postoperative AKI development have not been systematically compared after colorectal surgery.
Propofol (2,6-diisopropylphenol), which has antioxidant activity, is used widely for general anesthesia26 and inhibits the secretion of proinflammatory cytokines in septic animal models6,27–29 and during clinical sepsis.30 In a small 2014 study of cardiac surgery patients, propofol was associated with lower incidence of AKI than sevoflurane.12 In critically ill patients, propofol has also been associated with a lower risk of AKI than midazolam.31 The cause of AKI has been hypothesized to involve IR injury-induced or massive inflammation.12 One potential mechanism by which propofol might affect AKI incidence is by modulating the inflammatory response induced by IR injury and/or cardiopulmonary bypass and decreasing the concentration of inflammatory markers, such as renal myeloperoxidase, C-reactive protein, and proinflammatory cytokines, such as tumor necrosis factor-α, interleukin-1 and -6.11,12
In this study, the incidence of AKI was greater than that in previous studies of noncardiac surgeries,5,24 possibly because different AKI criteria were used. We also found that AKI incidence was greater in patients who had mechanical obstruction (24.1% and 16.1% by AKIN and RIFLE criteria, respectively) or ischemia (31.3% and 25.0% by AKIN and RIFLE criteria, respectively) of the bowel. Our results are consistent with animal data finding a relationship between bowel ischemia and renal function.32 Moreover, intestinal IR injury triggers multiorgan dysfunction and systemic inflammation.33,34 In addition, patients undergoing colorectal resection often receive mechanical bowel preparation,35 predisposing to volume depletion and, higher risk of AKI in patients who undergo colorectal surgery.36
In our study, after PS matching, sevoflurane was not associated with an increase in AKI using AKIN criteria (OR, 1.28; 95% CI, 0.99–1.67; P = 0.06) and only weakly associated with AKI using the RIFLE criteria (OR, 1.41; 95% CI, 1.02–1.95; P = 0.04). This discrepancy may be because AKIN criteria use a smaller change in sCr (0.3 mg/dL versus a percentage increase in sCr ≥ 50%) over a shorter time window (within 48 hours) than RIFLE criteria (within 7 days).37,38 A delayed increase in creatinine may thus trigger RIFLE, but not AKIN, metrics. Other studies have found discrepancies between AKIN and RIFLE in AKI incidence.
Another potential confounder may have been the greater use of sevoflurane for emergency surgery. Emergent operation is a strong predictor of postoperative AKI,24,25 and in our study, emergency patients had a higher ASA physical status, lower serum albumin level, required more diuretics, fluid administration, intraoperative pRBCs transfusion, and low intraoperative mean blood pressure; all risk factors of AKI.24 In addition, emergent patients were more frequently anesthetized with sevoflurane. Also, because the incidence of overall mortality of our study was low (1.9 %), a larger sample size may have better been able to detect the difference between 2 groups.
Our study has several limitations. First, because of its retrospective design, we could not control for all confounding parameters that might have affected our results. Although we performed PS analysis to control for selection bias, we could not entirely remove residual confounding. Second, because we enrolled patients with colorectal surgery, our results cannot be applied to other patient types, and care should be taken when interpreting our data.
In conclusion, when propensity matching is used, sevoflurane may be associated with a modest increase in the incidence of AKI when the RIFLE criteria but not AKIN criteria are used. Sevoflurane was not associated with an increase in mortality or ICU admission, and patients presenting for emergent surgery were at greater risk for AKI and more likely to be anesthetized with sevoflurane. Further large, multicenter, prospective trials are needed to establish such an association. E
Name: Ji-Yeon Bang, MD, PhD.
Contribution: This author helped conduct the study, analyze the data, and write the manuscript.
Name: JungBok Lee, PhD.
Contribution: This author helped analyze the data and Interpretation of data.
Name: Jimi Oh, MD
Contribution: This author helped analyze the data.
Name: Jun-Gol Song, MD, PhD.
Contribution: This author helped design the study, conduct the study, analyze the data, and write the manuscript.
Name: Gyu-Sam Hwang, MD, PhD.
Contribution: This author helped design the study and analyze the data.
This manuscript was handled by: Avery Tung, MD.
1. Kim M, Brady JE, Li GVariations in the risk of acute kidney injury across intraabdominal surgery procedures.Anesth Analg2014119112132
2. O’Connor ME, Kirwan CJ, Pearse RM, Prowle JRIncidence and associations of acute kidney injury after major abdominal surgery.Intensive Care Med2015
3. Chertow GM, Burdick E, Honour M, Bonventre JV, Bates DWAcute kidney injury, mortality, length of stay, and costs in hospitalized patients.J Am Soc Nephrol200516336570
4. Masoomi H, Carmichael JC, Dolich M, Mills S, Ketana N, Pigazzi A, Stamos MJPredictive factors of acute renal failure in colon and rectal surgery.Am Surg201278101923
5. Kheterpal S, Tremper KK, Heung M, Rosenberg AL, Englesbe M, Shanks AM, Campbell DA JrDevelopment and validation of an acute kidney injury risk index for patients undergoing general surgery: results from a national data set.Anesthesiology200911050515
6. Hsu BG, Yang FL, Lee RP, Peng TC, Chen HIEffects of post-treatment with low-dose propofol on inflammatory responses to lipopolysaccharide-induced shock in conscious rats.Clin Exp Pharmacol Physiol200532249
7. Yoo YC, Yoo KJ, Lim BJ, Jun JH, Shim JK, Kwak YLPropofol attenuates renal ischemia-reperfusion injury aggravated by hyperglycemia.J Surg Res201318378391
8. Hatakeyama N, Matsuda NAlert cell strategy: mechanisms of inflammatory response and organ protection.Curr Pharm Des201420576678
9. Liu S, Carpenter RL, Neal JMEpidural anesthesia and analgesia. Their role in postoperative outcome.Anesthesiology1995821474506
10. Schilling T, Kozian A, Senturk M, Huth C, Reinhold A, Hedenstierna G, Hachenberg TEffects of volatile and intravenous anesthesia on the alveolar and systemic inflammatory response in thoracic surgical patients.Anesthesiology20111156574
11. Sánchez-Conde P, Rodríguez-López JM, Nicolás JL, Lozano FS, García-Criado FJ, Cascajo C, González-Sarmiento R, Muriel CThe comparative abilities of propofol and sevoflurane to modulate inflammation and oxidative stress in the kidney after aortic cross-clamping.Anesth Analg20081063718
12. Yoo YC, Shim JK, Song Y, Yang SY, Kwak YLAnesthetics influence the incidence of acute kidney injury following valvular heart surgery.Kidney Int20148641422
13. Ye X, Lian Q, Eckenhoff MF, Eckenhoff RG, Pan JZDifferential general anesthetic effects on microglial cytokine expression.PLoS One20138e52887
14. Rodríguez-González R, Baluja A, Veiras Del Río S, Rodríguez A, Rodríguez J, Taboada M, Brea D, Álvarez JEffects of sevoflurane postconditioning on cell death, inflammation and TLR expression in human endothelial cells exposed to LPS.J Transl Med20131187
15. Kong HY, Zhu SM, Wang LQ, He Y, Xie HY, Zheng SSSevoflurane protects against acute kidney injury in a small-size liver transplantation model.Am J Nephrol20103234755
16. Eger EI II, Gong D, Koblin DD, Bowland T, Ionescu P, Laster MJ, Weiskopf RBDose-related biochemical markers of renal injury after sevoflurane versus desflurane anesthesia in volunteers.Anesth Analg199785115463
17. Higuchi H, Sumita S, Wada H, Ura T, Ikemoto T, Nakai T, Kanno M, Satoh TEffects of sevoflurane and isoflurane on renal function and on possible markers of nephrotoxicity.Anesthesiology19988930722
18. Polentarutti N, Picardi G, Basile A, Cenzuales S, Rivolta A, Matteucci C, Peri G, Mantovani A, Introna MInterferon-gamma inhibits expression of the long pentraxin PTX3 in human monocytes.Eur J Immunol199828496501
19. Levey AS, Bosch JP, Lewis JB, Greene T, Rogers N, Roth DA more accurate method to estimate glomerular filtration rate from serum creatinine: a new prediction equation. Modification of Diet in Renal Disease Study Group.Ann Intern Med199913046170
20. Yusuf S, Diener HC, Sacco RL, Cotton D, Ounpuu S, Lawton WA, Palesch Y, Martin RH, Albers GW, Bath P, Bornstein N, Chan BP, Chen ST, Cunha L, Dahlöf B, De Keyser J, Donnan GA, Estol C, Gorelick P, Gu V, Hermansson K, Hilbrich L, Kaste M, Lu C, Machnig T, Pais P, Roberts R, Skvortsova V, Teal P, Toni D, VanderMaelen C, Voigt T, Weber M, Yoon BWPRoFESS Study GroupTelmisartan to prevent recurrent stroke and cardiovascular events.N Engl J Med2008359122537
21. Austin PCA comparison of 12 algorithms for matching on the propensity score.Stat Med201433105769
22. Bang JY, Lee JB, Yoon Y, Seo HS, Song JG, Hwang GSAcute kidney injury after infrarenal abdominal aortic aneurysm surgery: a comparison of AKIN and RIFLE criteria for risk prediction.Br J Anaesth20141139931000
23. Alsabbagh MM, Asmar A, Ejaz NI, Aiyer RK, Kambhampati G, Ejaz AAUpdate on clinical trials for the prevention of acute kidney injury in patients undergoing cardiac surgery.Am J Surg20132068695
24. Kheterpal S, Tremper KK, Englesbe MJ, O’Reilly M, Shanks AM, Fetterman DM, Rosenberg AL, Swartz RDPredictors of postoperative acute renal failure after noncardiac surgery in patients with previously normal renal function.Anesthesiology2007107892902
25. Abelha FJ, Botelho M, Fernandes V, Barros HDeterminants of postoperative acute kidney injury.Crit Care200913R79
26. Murphy PG, Myers DS, Davies MJ, Webster NR, Jones JGThe antioxidant potential of propofol (2,6-diisopropylphenol).Br J Anaesth1992686138
27. Song XM, Wang YL, Li JG, Wang CY, Zhou Q, Zhang ZZ, Liang HEffects of propofol on pro-inflammatory cytokines and nuclear factor kappaB during polymicrobial sepsis in rats.Mol Biol Rep200936234551
28. Brasil LJ, San-Miguel B, Kretzmann NA, Amaral JL, Zettler CG, Marroni N, González-Gallego J, Tuñón MJHalothane induces oxidative stress and NF-kappaB activation in rat liver: protective effect of propofol.Toxicology20062275361
29. Runzer TD, Ansley DM, Godin DV, Chambers GKTissue antioxidant capacity during anesthesia: propofol enhances in vivo red cell and tissue antioxidant capacity in a rat model.Anesth Analg2002948993
30. Vanlersberghe C, Camu FPropofol.Handb Exp Pharmacol200818222752
31. Leite TT, Macedo E, Martins Ida S, Neves FM, Libório ABRenal outcomes in critically ill patients receiving propofol or midazolam.Clin J Am Soc Nephrol201510193745
32. LaNoue JL Jr, Turnage RH, Kadesky KM, Guice KS, Oldham KT, Myers SIThe effect of intestinal reperfusion on renal function and perfusion.J Surg Res1996641925
33. Kim M, Park SW, Kim M, D’Agati VD, Lee HTIsoflurane post-conditioning protects against intestinal ischemia-reperfusion injury and multiorgan dysfunction via transforming growth factor-β1 generation.Ann Surg2012255492503
34. Clark JA, Coopersmith CMIntestinal crosstalk: a new paradigm for understanding the gut as the “motor” of critical illness.Shock20072838493
35. Guenaga KF, Matos D, Wille-Jorgensen PMechanical bowel preparation for elective colorectal surgery.Cochrane Database Syst Rev2011Cd001544
36. Choi NK, Lee J, Chang Y, Jung SY, Kim YJ, Lee SM, Lee JH, Kim JY, Song HJ, Park BJPolyethylene glycol bowel preparation does not eliminate the risk of acute renal failure: a population-based case-crossover study.Endoscopy20134520813
37. Mehta RL, Kellum JA, Shah SV, Molitoris BA, Ronco C, Warnock DG, Levin AAcute Kidney Injury NetworkAcute Kidney Injury Network: report of an initiative to improve outcomes in acute kidney injury.Crit Care200711R31
38. Joannidis M, Metnitz B, Bauer P, Schusterschitz N, Moreno R, Druml W, Metnitz PGAcute kidney injury in critically ill patients classified by AKIN versus RIFLE using the SAPS 3 database.Intensive Care Med2009351692702