Endothelial Dysfunction in Kidney Transplantation

Front Immunol. 2018 May 23;9:1130. doi: 10.3389/fimmu.2018.01130. eCollection 2018.

Abstract

Kidney transplantation entails a high likelihood of endothelial injury. The endothelium is a target of choice for injury by ischemia-reperfusion, alloantibodies, and autoantibodies. A certain degree of ischemia-reperfusion injury inevitably occurs in the immediate posttransplant setting and can manifest as delayed graft function. Acute rejection episodes, whether T-cell or antibody-mediated, can involve the graft micro- and macrovasculature, leading to endothelial injury and adverse long-term consequences on graft function and survival. In turn, caspase-3 activation in injured and dying endothelial cells favors the release of extracellular vesicles (apoptotic bodies and apoptotic exosome-like vesicles) that further enhance autoantibody production, complement deposition, and microvascular rarefaction. In this review, we present the evidence for endothelial injury, its causes and long-term consequences on graft outcomes in the field of kidney transplantation.

Keywords: alloantibodies; apoptosis; autoantibodies; endothelial injury; kidney transplantation; necroptosis.

Publication types

  • Research Support, Non-U.S. Gov't
  • Review

MeSH terms

  • Animals
  • Autoimmunity
  • Endothelial Cells / metabolism
  • Endothelium / metabolism*
  • Endothelium / pathology
  • Endothelium / physiopathology
  • Graft Rejection / immunology
  • Graft Survival / immunology
  • Humans
  • Kidney Transplantation / adverse effects*
  • Microvascular Rarefaction / metabolism
  • Microvascular Rarefaction / pathology
  • Reperfusion Injury / etiology
  • Reperfusion Injury / metabolism
  • Reperfusion Injury / pathology
  • Reperfusion Injury / physiopathology
  • Vascular Remodeling