Effect of brain death on gene expression and tissue activation in human donor kidneys

Autor: Janneke Wiersema-Buist, Henri G. D. Leuvenink, Susan Fekken, Willem J. van Son, Jaap J. Homan van der Heide, Sijbrand Hofker, Joost A. B. van der Hoeven, Theo A. Schuurs, Willemijn N. Nijboer, Rutger J. Ploeg
Přispěvatelé: Surgery, Other departments, Faculteit Medische Wetenschappen/UMCG, Groningen Institute for Organ Transplantation (GIOT)
Jazyk: angličtina
Rok vydání: 2016
Předmět:
Zdroj: Transplantation, 78(7), 978-986. Lippincott Williams and Wilkins
Transplantation, 78(7), 978-986. LIPPINCOTT WILLIAMS & WILKINS
ISSN: 0041-1337
Popis: Background. After kidney transplantation, decreased graft survival is seen in grafts from brain dead (BD) donors compared with living donors. This might result partly from a progressive nonspecific inflammation in the graft. In this study, we focused on the effects of BD on inflammatory response (adhesion molecules, leukocyte invasion, gene expression) and stress-related heat shock proteins in the human kidney. Research outcomes and clinical donor parameters were then linked to outcome data after transplantation.Methods. Kidney biopsy specimens and serum were obtained during organ retrieval from BD and living organ donor controls. Immunohistochemistry and semquantitative reverse transcriptase-polymerase chain reaction were performed on the biopsy specimens. Clinical and laboratory parameters from BD donors were recorded and connected to outcome data of the recipients of the kidneys studied.Results. After brain death, immunohistochemistry showed an increase of E-selectin (P Conclusions. The presence of interstitial leukocytes and the early adhesion molecule E-selectin in BD donor kidneys indicates an early-phase inflammatory process during organ retrieval. Elevated levels of monocyte chemotactic protein-1 and transforming growth factor-beta suggest a role for monocytes/macrophages in this phase. We suggest that BD causes a stress-related response against which protective heat shock proteins are formed in the future graft. This stress response may be too severe to be fully counteracted by elevated heat shock proteins. Which systemic and/or local factors trigger brain death-related graft injury is currently under investigation.
Databáze: OpenAIRE