Intraoperative Oliguria: Physiological or Beginning Acute Kidney Injury?

Acute kidney injury (AKI) is a serious complication with a huge impact on patients’ outcome. In abdominal surgery, the incidence of AKI is about 13%1 and is associated with increased morbidity, an 8-fold increased risk for the development of chronic kidney disease,2 and a 13-fold increased relative risk of in-hospital or 30-day mortality.1 According to the guidelines from the Kidney Disease: Improving Global Outcomes (KDIGO), AKI is defined by changes in serum creatinine and/or urine output.3 Although urine output is an unspecific marker of kidney function, it has been shown that a reduced urine output is associated with a worse outcome in critically ill patients.4 However, several studies investigating the association between intraoperative urine output and postoperative AKI have shown that a reduced intraoperative urine output does not predict postoperative AKI.1,5 Urine output may be influenced by hemodynamics, intravascular hypovolemia/hypervolemia, and hormone levels (aldosterone and antidiuretic hormone). Anesthetic agents, especially volatile anesthetics, have the potential to decrease renal blood flow, glomerular filtration rate, and renal tubular function.6 Moreover, during laparoscopic procedures, an increased intraabdominal pressure contributes to a reduction in urine output, however, not necessarily reflecting an AKI.7 Therefore, the reliability of urine output is extensively debated. However, because an early implementation of preventive strategies can reduce the incidence of AKI, it is of high interest to find an early predictor for AKI. In this issue of Anesthesia & Analgesia, Shiba et al8 investigated whether intraoperative oliguria is associated with postoperative AKI after major noncardiac surgery. The authors showed in 5894 patients undergoing major noncardiac surgery that intraoperative oliguria (defined as urine output <0.5 mL/kg/h for ≥120 minutes) was independently associated with the development of AKI as defined by an increase in serum creatinine levels, even after adjusting for confounding factors. The overall incidence of AKI was 7.3% (n = 429; 15.6% in patients with ≥120 minutes oliguria versus 5.9% in patients with <120 minutes oliguria; odds ratio, 2.104; P < .001). Moreover, they demonstrated that a longer duration of oliguria is associated with a higher risk for developing AKI (odds ratio, 12.353 in patients with ≥300 minutes of oliguria; P < .001). The results of this retrospective analysis are in line with data from Mizota et al.9 They performed a retrospective analysis in 3560 patients undergoing major abdominal surgeries and found an association between oliguria and AKI, especially at a threshold of ≤0.3 mL/kg/h.9 However, Mizota et al9 did not show a correlation at a threshold of 0.3–0.5 mL/kg/h. The difference between both studies is the use of diuretics, which was an exclusion criterion in the analysis by Mizota et al.9 The results suggest that the intraoperative oliguria threshold needs to be individualized depending on the underlying condition (patients’ comorbidities, medication, and surgical procedure). For example, in cardiac surgical patients, a threshold of 1.5 mL/kg/h is suggested during cardiopulmonary bypass.10 In major abdominal surgeries, the use of diuretics might lead to higher intraoperative urine output threshold as compared with patients not receiving diuretics. However, to proof this mechanism, large observational trials are needed. But why is an early recognition of a developing AKI important? In clinical routine, oliguria is easy to monitor especially in patients undergoing major surgeries who frequently have a Foley catheter. Knowing that intraoperative oliguria may be an early marker for AKI, preventive strategies could be initiated at an early stage. However, caution is advised when interpreting the results. Inappropriate interpretation of oliguria may lead to inappropriate fluid administration in an attempt to improve urine output. This might be harmful since it is well known that fluid overload itself is independently associated with the development of AKI,11 postoperative complications,12 longer hospital length of stay,12 and mortality.13 The underlying pathophysiology resulting in AKI is based on the development of tissue edema caused by fluid overload, and this subsequently results in obstruction of capillary blood flow in encapsulated organs such as the kidneys, and increases in interstitial pressure.14 Especially in patients undergoing laparoscopic procedures, the use of urine output as trigger for fluid therapy cannot be recommended.15 On the other hand, reduced urine output caused by hypovolemia affects hemodynamics and reduces renal perfusion provoking AKI. Consequently, an individualized approach is deemed necessary and an adequate monitoring of fluid balance of high importance. There are already some studies showing that an algorithm-based approach to optimize the hemodynamic situation reduced the occurrence of AKI and improves patients’ outcome.16,17 It remains an unsolved problem that monitoring serves as the optimal tool for management of fluid application. This needs to be addressed in subsequent studies. What we need for the future is an ideal renal biomarker that guides clinicians in the decision-making process. Considerable effort has already been made to find such a “troponin-equivalent” marker for the kidneys. Recently, cell cycle arrest markers have been the focus of interest since they have shown promising results for identifying patients at high risk for AKI in different settings and early implementation of preventive strategies.16,17 In oliguric patients, an early marker of kidney damage that differentiates between imminent AKI and physiological reaction would be helpful for clinicians to improve patients’ outcome. DISCLOSURES Name: Mira Küllmar, MD. Contribution: This author helped prepare the manuscript. Conflicts of Interest: None. Name: Melanie Meersch, MD. Contribution: This author helped prepare and review the manuscript. Conflicts of Interest: M. Meersch received lecture fees from Astute Medical and Baxter. This manuscript was handled by: Alexander Zarbock, MD.