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Author Notes:

Corresponding author contact information: Andres Pelaez, MD, Emory University School of Medicine, Ste F-520, 1364 Clifton Rd NE, Atlanta, GA 30322, Office: 404-727-9651, Fax: 404-727-1516, apelaez@emory.edu.

The authors wish to thank Dr Steven R. Duncan at the University of Pittsburgh for his assistance editing the manuscript, LifeLink Foundation (organ procurement organization) and Jennifer Smith (Department of Pathology, Emory University Hospital) for their assistance.


Research Funding:

F32 NRSA to POM (5F32AA016262)

Emory University Research Council award to AP (2006073)

Emory Alcohol Lung and Biology Center (NIH NIAAA, 1P50AA13575701)


  • Science & Technology
  • Life Sciences & Biomedicine
  • Surgery
  • Transplantation
  • Lung transplantation
  • primary graft dysfunction
  • receptor for advanced glycation end products
  • RAGE
  • reperfusion injury

Receptor for Advanced Glycation End Products in Donor Lungs Is Associated with Primary Graft Dysfunction After Lung Transplantation

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Journal Title:

American Journal of Transplantation


Volume 10, Number 4


, Pages 900-907

Type of Work:

Article | Post-print: After Peer Review


Development of primary graft dysfunction (PGD) is associated with poor outcomes after transplantation. We hypothesized that Receptor for Advanced Glycation End-products (RAGE) levels in donor lungs is associated with the development of PGD. Furthermore, we hypothesized that RAGE levels would be increased with PGD in recipients after transplantation. We measured RAGE in bronchoalveolar lavage fluid (BALf) from 25 donors and 34 recipients. RAGE was also detected in biopsies (TBBX) from recipients with and without PGD. RAGE levels were significantly higher in donor lungs that subsequently developed sustained PGD vs transplanted lungs that did not display PGD. Donor RAGE level was a predictor of recipient PGD (odds ratio = 1.768 per 0.25 ng/ml increase in donor RAGE level). In addition, RAGE levels remained high at 14 days in those recipients that developed severe graft dysfunction. Recipients may be at higher risk for developing PGD if they receive transplanted organs that have higher levels of soluble RAGE prior to explantation. Moreover, the clinical and pathologic abnormalities associated with PGD post-transplantation are associated with increased RAGE expression. These findings also raise the possibility that targeting the RAGE signaling pathway could be a novel strategy for treatment and/or prevention of PGD.

Copyright information:

© 2010 The American Society of Transplantation and the American Society of Transplant Surgeons.

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