RT Book, Section A1 Giangola, Matthew A1 Kuncewitch, Michael A1 Wang, Ping A2 Molmenti, Ernesto Pompeo SR Print(0) ID 1194188498 T1 Ischemia Reperfusion T2 Molmenti’s Kidney and Pancreas Transplantation: Operative Techniques and Medical Management, 2e YR 2023 FD 2023 PB McGraw Hill PP New York, NY SN 9781260474275 LK accesssurgery.mhmedical.com/content.aspx?aid=1194188498 RD 2024/11/11 AB Renal ischemia-reperfusion (I/R) injury involves several complex pathophysiological mechanisms that are incompletely understood. Broadly, cellular injury is in part due to the anoxic cell death incurred during the ischemic period, as well as the buildup of free radicals. However, with the return of blood flow comes an accumulation of inflammatory cells and mediators, reactive oxygen species (ROS) and reactive nitrogen species (RNS). The subsequent biochemical derangements in intracellular homeostasis trigger a cascade to further cell death from inflammation, apoptosis, and necrosis.1,2 These events may lead to delayed graft function in the case of transplant recipients or increases in complications, length of hospital stay, and cost of care for those experiencing I/R injury. Currently, the clinical diagnosis of acute kidney injury due to renal I/R is both difficult to confirm and likely comprised of multiple pathologies.3 Clinical indicators of renal injury range from serum creatinine, serum and urine electrolytes, fractional excretion of sodium, neutrophil gelatinase–associated lipocalin, and urine microscopy.4 The following chapter provides a cellular overview of the I/R inflammatory process and lists potential clinical biomarkers to detect clinically significant injury.