The effect of perioperative AKI on surgical outcomes

Abstract

Postoperative acute kidney injury (AKI) is a common complication that is associated with development of chronic kidney failure, prolonged hospitalization and increased mortality. The occurrence rate ranges from 10 to 47% in high-risk surgeries and patients [1]. The etiol-ogy and mechanisms are complex and multifactorial. It has been suggested that even small rises in creatinine (≥ 0.3 mg/dl) are independently related to an approximately fourfold increase in hospital mortality. Hence, it is important to identify the risk factors and the patho-physiology of AKI to develop the strategies to prevent and treat AKI. In this issue of the journal, Mok and colleagues summarize the pathophysiology, treatment, and surgical outcomes of perioperative AKI, and discuss updated measures of AKI prevention and treatment. This review describes the three main definitions of AKI: the Risk, Injury, Failure, Loss and End-stage kidney disease (RIFLE) criteria, the Acute Kidney Injury Network (AKIN) criteria and the Kidney Disease: Improving Global Outcomes (KDIGO) criteria. Even though the 2012 KDIGO task force offers a cohesive interpretation of RIFLE and AKIN criteria, there is still no consensus on which criteria is more accurate in evaluating AKI. Mok and colleagues also break down common etiologies of AKI into prerenal, renal and postrenal causes (Fig. 1). If the etiology of AKI can be reversed rapidly, renal function can generally be recovered. The kidney is regarded as a highly vascularized organ, characterized by a remarkable diversity of endothelial cell populations. The function of endothelial cells is increasingly well understood. Molitoris and colleagues describe the renal vascular endothelium as a dynamic organ, which promotes an antithrombotic and anti-inflamma-tory environment and maintains tissue perfusion and vascular tone under physiological conditions. Impairment of these vital endothelial cell functions contributes to reduced renal perfusion, continued renal hypoxia, and the subsequent diminution in glomerular filtration rate that is the feature of AKI. Mok and colleagues also describe the causes of renal vascular endothelial cell injury, including hypoxia, ischemia or nephrotoxicity. Those pathophysiological processes can be triggered and occur in specific AKI cases simultaneously. This review describes that up to 60% of in-hospital AKI cases are caused by drug-induced nephrotoxicity which includes non-steroidal anti-inflammatory drugs (NSAIDs), ami-noglycoside antibiotics and intravenous imaging contrast agents, which should be taken into account in the periop-erative management of patients. Mok and colleagues further discussed periopera-tive risk factors for AKI. During the intraoperative period, patients who underwent emergency surgery, large volume of blood loss and blood transfusion, redo surgery, such as liver transplant, more complex procedures, longer surgery duration, and longer car-diopulmonary bypass (CPB) time are predisposed to develop AKI. Therefore, more studies have focused on major surgical procedures such as cardiac surgery and CPB. In fact, special types of surgeries involving major vascular and renal vascular operations, such as liver