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 2024/04/19
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.