Postoperative Acute Kidney Injury

Abstract

Postoperative AKI is a common complication of major surgery and is associated with significant morbidity and mortality. The Kidney Disease Improving Global Outcomes AKI definition allows consensus classification and identification of postoperative AKI through changes in serum creatinine and/or urine output. However, such conventional diagnostic criteria may be inaccurate in the postoperative period, suggesting a potential to refine diagnosis by application of novel diagnostic biomarkers. Risk factors for the development of postoperative AKI can be thought of in terms of preoperative, intraoperative, and postoperative factors and, as such, represent areas that may be targeted perioperatively to minimize the risk of AKI. The treatment of postoperative AKI remains predominantly supportive, although application of management bundles may translate into improved outcomes.

Keywords: Critical Care Nephrology and Acute Kidney Injury Series; acute kidney injury; biomarkers; kidney replacement therapy; perioperative; postoperative; surgery.

Figure 1.

Pathophysiology of postoperative AKI. Postoperative AKI often has a multifactorial etiology mediated by common injury pathways that affect the kidney microcirculation, oxygen (O₂) demand, and inflammation. In most cases, a combination of preoperative risk factors, intraoperative events, and postoperative events leads to the development of AKI. Baseline risk factors and the persistence and severity of injurious factors in the postoperative setting also determine the outcomes of AKI, acute kidney disease, and, eventually, CKD. Adapted from ref. , with permission.

Figure 2.

Major pathophysiologic processes contributing to AKI after vascular and cardiac surgery. Hemodynamic perturbations occur because of nonpulsatile flow due to bypass therapy, crossclamping of the aorta, inovasopressor treatment, and volume resuscitation. More specific mechanical causes can also lead to AKI, such as microembolic phenomena, which occur because of cardiopulmonary bypass (CPB). Similarly, volume overload or right heart failure with venous congestion can compromise kidney function; mechanisms here are yet to be elucidated but may relate to “back pressure” on the glomerulus. Tubular toxicity can also occur as a result of the direct effects from free hemoglobin and liberation of free iron. This, alongside multiple other mechanisms, such as cholesterol emboli from crossclamping, blood transfusion, and immune activation from blood-bypass circuit interactions, can increase oxidative stress and lead to activation of inflammatory pathways. Reprinted from ref. , with permission.