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Cold Ischemic Injury of Organs for Transplantation: Devastation,
Mechanisms and Prevention
American Federation of Medical Researchers
Abdulla Salahudeen and Kenneth B. Storey
Speakers: Abdulla K. Salahudeen, Kenneth B. Storey, Hamid Rabb, F.J.
VanderWoud and
Ursula Rauen
Cadaver organs are
routinely cold stored while awaiting transplantation. The average cold
ischemia time (CIT) for kidney in US is still 18-24 hrs according to the
latest United Network of Organs Sharing (UNOS) data. Such extended CIT is
detrimental to the allografts and recipients in the short term. Recent UNOS
data analysis from our group shows that extended CIT is also detrimental to
the long-term survival of renal allograft. So, if cold storage is bad, can
we do away with cold storage? The short answer is, not for now. For one,
cold storage allows better tissue matching, which confers some survival
advantage. Whether such advantage off sets the negative effect of cold
ischemia is however, debatable. Now that cold storage is here to stay for
now, more need to be done to protect the organs against cold ischemic
injury. Cold storage injury is potentially “intervenable” as most organ
retrievals are carried out as an elective procedure, thus, providing
opportunity to precondition or pretreat the organs prior to cold ischemia.
As it stands, the “art” of cold storage is pretty much stuck in the 80s when
Belzar and Southard introduced the University of Wisconsin (UW) solution.
The good news is that a number of groups have been working on understanding
the molecular and cellular mechanisms of cold ischemic injury. However, to
best of my knowledge, few meetings, including Transplantation Conferences,
have recognized or addressed this in any serious way. This provides us an
opportunity to propose a symposium
entitled “Cold ischemic injury of organs for transplantation: devastation,
mechanisms and prevention” at the
AFMR-Experimental Biology 2004 meeting.
The objective will be to recognize cold ischemic injury as an
important mediator of short and probably long term allograft damage and
attrition so as the clinicians and scientists can discuss possible ways to
limit this form of injury in the light of newer cellular and molecular
mechanisms.
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