Elsevier

Transplantation Proceedings

Volume 29, Issues 1–2, February–March 1997, Pages 79-81
Transplantation Proceedings

The “injury response”: A concept linking nonspecific injury, acute rejection, and long-term transplant outcomes

https://doi.org/10.1016/S0041-1345(96)00015-2Get rights and content

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References (22)

  • D.A. Shoskes et al.

    J Urol

    (1996)
  • F. Sanfilippo et al.

    Transplantation

    (1984)
  • P.F. Halloran et al.

    transplantation

    (1988)
  • P.F. Halloran et al.

    Transplantation

    (1988)
  • J.S. Najarian et al.

    Transplantation

    (1994)
  • T. Cacciarelli et al.

    Clin Nephrol

    (1993)
  • K. Solez et al.

    Acute Renal Failure: Diagnosis, Treatment and Prevention

  • P.F. Halloran et al.
  • P.I. Terasaki et al.

    N Engl J Med

    (1995)
  • B.M. Brenner et al.

    J Am Soc Nephrol

    (1992)
  • A.C. Gulanikar et al.

    Transplantation

    (1992)
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      In this study, taking into account the paired origin of the grafts, we analyzed CIT and its consequences. CIT has been shown to be an independent risk factor for DGF, but the “best” CIT is still controversial [1–9,12,13–16]. In this study, we found that CIT > 20 hours is a risk factor for DGF, in agreement with other studies [1,2,5,9,15].

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      Interestingly, despite activation of caspase-1, we see no evidence of IL-1β activity in necrotic EC lysates, suggesting that ECs either do not express pro-IL-1β or that it is compartmentalized away from the caspase-1 activity. These and previous data (6, 7) also suggest that the burden of injury hypothesis (3) and the immune modulation hypothesis (1) of graft rejection cannot be mutually exclusive. Necrotic ECs cannot activate IL-1α without initial damage to vessels that cause release of active IL-1α from VSMCs or other sources, However, once primed, ECs can subsequently activate IL-1α upon necrosis and in addition up-regulate adhesion molecules such as intercellular adhesion molecule 1 and E-selectin, leading to recruitment of leukocytes.

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    Supported by the Medical Research Council of Canada, Kidney Foundation of Canada, Sandoz Canada, Hoffmann-La Roche, Royal Canadian Legion, and Muttart Foundation.

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