gms | German Medical Science

126. Kongress der Deutschen Gesellschaft für Chirurgie

Deutsche Gesellschaft für Chirurgie

28.04. - 01.05.2009, München

Cell-based therapy using endothelial progenitor cells rescues kidney from transplantation-induced ischemia-reperfusion injury

Meeting Abstract

  • corresponding author T. Herrler - Chirurgische Klinik, Campus Großhadern, LMU München
  • A. Tischer - Chirurgische Klinik, Campus Großhadern, LMU München
  • S. Nowak - Nuklearmedizinische Klinik, LMU München
  • S.F. Leicht - Chirurgische Klinik, Campus Großhadern, LMU München
  • T. Schwarz - Chirurgische Klinik, Campus Großhadern, LMU München
  • P. Bartenstein - Nuklearmedizinische Klinik, LMU München
  • M. Hacker - Nuklearmedizinische Klinik, LMU München
  • C. Heeschen - Chirurgische Klinik, Campus Großhadern, LMU München

Deutsche Gesellschaft für Chirurgie. 126. Kongress der Deutschen Gesellschaft für Chirurgie. München, 28.04.-01.05.2009. Düsseldorf: German Medical Science GMS Publishing House; 2009. Doc09dgch10784

doi: 10.3205/09dgch294, urn:nbn:de:0183-09dgch2940

Published: April 23, 2009

© 2009 Herrler et al.
This is an Open Access article distributed under the terms of the Creative Commons Attribution License ( You are free: to Share – to copy, distribute and transmit the work, provided the original author and source are credited.



Introduction: In the past years, optimization of immunosuppressive protocols considerably reduced the incidence of acute rejection after kidney transplantation. In contrast, very little progress has been achieved in the field of long-term transplant function and survival. Chronic allograft dysfunction still represents a major cause of graft loss and the underlying multi-factorial reasons involving both immunological and non-immunological aspects remain poorly understood. In the clinical setting prevention of ischemia-reperfusion injury as an non-immunological factor is achieved by cold preservation and particular perfusion solutions, whereas effective renoprotective treatment options after transplantation are still lacking. As prolonged ischemia not only leads to early tissue damage with reduced graft function, but also exhibits deteriorating long-term effects on the transplant kidney by increasing immunogenicity and predisposition to fibrosis, we aimed to identify new treatment strategies to counter or even reverse this clinical disease pattern.

Material and methods: The precise part of different renal structures and components in kidney dysfunction and the effects of endothelial progenitor cell therapy were analyzed in a murine model of ischemia-reperfusion injury using 99mTc-MAG3 scintigraphy, assessment of laser Doppler perfusion, examination of kidney-relevant parameters in blood and urine, as well as histological analysis.

Results: Without treatment, ischemia-reperfusion injury exhibited a substantial reduction of renal function with no evidence for regeneration, considerable tissue damage, and marked impairment of organ perfusion. Progenitor cell therapy potently enhanced vascular regeneration with increased perfusion and excellent tissue vitality, but had only limited beneficial effect on functional impairment. Histological analysis conclusively confirmed functional findings.

Conclusion: Here, we show that cell-based therapy using endothelial progenitor cells represents a promising strategy to suspend the deteriorating cascade of events following ischemia-reperfusion injury. This novel treatment modality may aid to prolong allograft function and survival after kidney transplantation.