In this study, we found that, in patients who underwent open MAS, the type of anesthetic used had a significant effect on the likelihood of postoperative AKI, as defined by KDIGO criteria. The risk for postoperative AKI was 1.7-fold higher in patients who underwent inhalational anesthesia using sevoflurane or desflurane compared to those receiving propofol-based anesthesia; the score analysis and IPTW confirmed this finding. Moreover, all stages of AKI were more frequent in inhalant-based anesthesia than in propofol-based anesthesia.
In most cases, the choice of anesthetic agent is still based largely on the preference of the attending anesthesiologist, as no agent is known to be definitively superior to the others in terms of patient outcomes, except in specific contexts such as neurosurgical anesthesia.(24) Recent research on the relationship between anesthetics and postoperative outcomes, including long-term survival, has centered on the field of ‘onco-anesthesia’.(25) Numerous studies have assessed the effects of anesthetics on mortality after various types of cancer surgeries.(26–29). Although large randomized controlled trials are still required, a significant difference in the risk of mortality according to the anesthetic used in patients undergoing cancer surgery has been reported by previous studies.(26–28) Against this background, it seems clear that, to optimize outcomes, the choice of anesthetic should be based on the characteristics of the individual case rather than the anesthesiologist’s discretion. However, the literature on this topic is currently insufficient.
Postoperative AKI is a frequent complication associated with increased medical expenses.(30) Thus, prevention of postoperative AKI is important, and many studies have been performed to identify potential risk factors and construct prediction models. Previous studies typically enrolled patients undergoing cardiac surgery, among whom the incidence of postoperative AKI is exceptionally high.(31–36) These studies included numerous variables in their prediction models, such as older age, higher BMI, impaired preoperative renal function, hypertension, diabetes mellitus, chronic obstructive pulmonary disease, emergent surgery, and prolonged duration of cardiopulmonary bypass.(31–36) However, none of the models considered the type of anesthetic as a risk factor for AKI, and few studies were performed in a non-cardiac surgery setting. In the present study, we found that the type of anesthetic may significantly affect the likelihood of AKI following major non-cardiac surgery.
Propofol has attracted the attention of researchers due to its organ-protective effects (exerted via anti-inflammatory and immune-modulatory actions) and anti-oxidant properties.(37, 38) In vivo studies showed that propofol attenuated tissue injury by reducing susceptibility to oxidative stress and improving anti-oxidant capacity.(11, 39) Inhalational anesthetics are also known to confer organ protection by attenuating inflammation, necrosis, and apoptosis in vivo.(14, 40) Based on such findings, several clinical studies evaluated the renoprotective effects of anesthetics.(15, 16, 18) Yoo and colleagues showed that patients who received propofol anesthesia had a significantly lower risk of AKI following valvular heart surgery than those who received sevoflurane anesthesia.(16) They also showed that propofol suppressed the release of inflammatory cytokines such as interleukin (IL)-1, IL-6, and tumor necrosis factor-α. In terms of major non-cardiac surgery, Bang and co-workers observed a lower incidence of AKI after colorectal surgery with propofol- than with sevoflurane-based anesthesia.(15) In contrast, a recent study found no significant difference in the incidence of AKI between propofol- and sevoflurane-based anesthesia after lung resection surgery.(18) However, the results of previous studies lack generalizability and cannot be extrapolated to all types of major non-cardiac surgery. In our study, we included patients who underwent not only colorectal surgery but also gastrectomy, hepatectomy, and pancreatectomy, and found that propofol may be more advantageous than inhalational anesthetics in terms of preventing postoperative AKI.
The present study has several limitations. First, it used a retrospective design, and although numerous potential confounders were adjusted for in the multivariable model, the results should only be considered as a source of hypotheses; the causal relationship between type of anesthetic and postoperative AKI could not be established. Second, although we performed two additional logistic regression analyses after propensity score matching and IPTW to strengthen our findings, the results may have been biased to some degree. Third, postoperative measurement of SCr was not mandatory; thus, given that patients with more comorbidities are typically tested more frequently, the incidence of postoperative AKI may have been biased. Fourth, we did not define AKI based on the urine output criteria of KDIGO, and the hourly urine output data in the electronic medical records may have been inaccurate because they were recorded manually. Thus, the incidence of AKI may have been underestimated.
In conclusion, the type of anesthetic can have an independent and significant effect on the likelihood of AKI after open MAS. Patients undergoing inhalational anesthesia using sevoflurane or desflurane may be more prone to postoperative AKI than those anaesthetized with propofol. Large, well-controlled randomized trials should be performed to further investigate this association.