Source:http://linkedlifedata.com/resource/pubmed/id/19100389
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Predicate | Object |
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rdf:type | |
lifeskim:mentions | |
pubmed:issue |
10
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pubmed:dateCreated |
2008-12-22
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pubmed:abstractText |
Chemokines are involved in the recruitment of inflammatory cells to vascularized allografts. The chemokine CCL2/MCP-1 is expressed during allograft dysfunction, which is associated with the recruitment of inflammatory cells. Both intrinsic renal cells (donor origin) as well as infiltrating inflammatory cells (recipient origin) can be a source of CCL2/MCP-1. We previously demonstrated that the recipient MCP-1-2518G polymorphism is associated with increased CCL2/MCP-1 production by inflammatory cells and decreased renal allograft survival. We evaluated the impact of the MCP-1-2518G polymorphism in donor cells on renal allograft outcomes. We enrolled 252 recipients of kidney allografts in this retrospective study who had received grafts from 152 cadaveric donors. The CCL2/MCP-1 genotype was assessed using genomic DNA isolated from cryopreserved donor splenocytes. Outcome parameters studied were acute biopsy proven rejection (Banff criteria), serum creatinine, and glomerular filtration rate (GFR) at 1 year after transplantation, allograft loss, and death. MCP-1-2518 genotypes were in HW equilibrium. A/A was present in 125 (49.6%), A/G in 107 (42.5%), and G/G in 20 (7.9%) donor kidneys. There were no significant differences in the number of rejection episodes, the number of allograft losses, serum creatinine, GFR, or overall survival 1 year after transplantation. In contrast with the detrimental effect of the CCL2/MCP-1 polymorphism of the recipient, the CCL2/MCP-1 polymorphism of the donor has no impact on the allograft outcome during the first year after transplantation. The impact on the long-term outcomes needs further evaluation.
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pubmed:language |
eng
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pubmed:journal | |
pubmed:citationSubset |
IM
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pubmed:chemical | |
pubmed:status |
MEDLINE
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pubmed:month |
Dec
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pubmed:issn |
0041-1345
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pubmed:author | |
pubmed:issnType |
Print
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pubmed:volume |
40
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
3359-61
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pubmed:meshHeading |
pubmed-meshheading:19100389-Chemokine CCL2,
pubmed-meshheading:19100389-Chemokines,
pubmed-meshheading:19100389-DNA Primers,
pubmed-meshheading:19100389-Follow-Up Studies,
pubmed-meshheading:19100389-Glomerular Filtration Rate,
pubmed-meshheading:19100389-Humans,
pubmed-meshheading:19100389-Kidney Transplantation,
pubmed-meshheading:19100389-Polymorphism, Single Nucleotide,
pubmed-meshheading:19100389-Restriction Mapping,
pubmed-meshheading:19100389-Retrospective Studies,
pubmed-meshheading:19100389-Transplantation, Homologous,
pubmed-meshheading:19100389-Treatment Outcome
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pubmed:year |
2008
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pubmed:articleTitle |
The source matters: no impact of the CCL2/MCP-1-1-2518G polymorphism of the donor on renal allograft outcome during the first year after transplantation.
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pubmed:affiliation |
Medizinische Poliklinik, Campus Innenstadt, University of Munich, Germany.
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pubmed:publicationType |
Journal Article,
Research Support, Non-U.S. Gov't
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