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Kidneys derived from brain death organ donors show an inferior survival when compared to kidneys derived from living donors. Brain death is known to induce organ injury by evoking an inflammatory response in the donor. Neuronal injury triggers an inflammatory response in the brain, leading to endothelial dysfunction and the release of cytokines in the circulation. Serum levels of interleukin-6, -8, -10, and monocyte chemoattractant protein-1 (MCP-1) are increased after brain death. Binding with cytokine-receptors in kidneys stimulates activation of nuclear factor-kappa B (NF-kappaB), selectins, adhesion molecules and production of chemokines leading to cellular influx. Mitogen-activated protein kinases (MAP-kinases) mediate inflammatory responses and together with NF-kappaB they seem to play an important role in brain death induced renal injury. Altering the activation state of MAP-kinases could be a promising drug target for early intervention to reduce cerebral injury related donor kidney damage and improve outcome after transplantation.

Original publication

DOI

10.1111/j.1600-6143.2009.02587.x

Type

Journal article

Journal

Am J Transplant

Publication Date

05/2009

Volume

9

Pages

989 - 997

Keywords

Blood-Brain Barrier, Brain Death, Chemokines, Endothelium, Vascular, Extracellular Signal-Regulated MAP Kinases, Humans, Inflammation, Kidney, Kidney Transplantation, Neurons, Signal Transduction, Tissue Donors, Transcription, Genetic