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pubmed-article:15084179pubmed:abstractTextTissue attenuates to injury by the effects of heme oxygenase (HO)-1. The induction of HO-1 expression is modulated by a (GT)(n) dinucleotide polymorphism in the promoter of the gene, of which increased activity is associated with short (S) (<or=27) repeats. We investigated the influence of this HO-1 gene polymorphism on renal transplant survival. DNA from 387 recipients and 384 donors was genotyped and we divided the HO-1 alleles into two subclasses, the S (<or=27 repeats) class and long (L) class (>27 repeats). Graft survival was associated with donor and not with recipient HO-1 gene polymorphism (log rank p = 0.005; hazard ratio 0.51, 95% CI 0.32-0.83). The beneficial effect of the donor HO-1 genotype was observed in grafts exposed to prolonged cold ischemia time and acute rejection. Patients who received a kidney from L-homozygotes lost their graft significantly more often to chronic allograft nephropathy (CAN) than carriers of S-alleles (p = 0.015). Multivariate analysis showed reduced risk for graft failure in kidneys with S-alleles in comparison to L-homozygotes (odds ratio 0.50, 95% CI 0.27-0.93, p = 0.03). Kidneys that are carriers of HO-1 S-allele are less vulnerable to tissue injury resulting in less CAN and better graft survival.lld:pubmed
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pubmed-article:15084179pubmed:authorpubmed-author:ClaasFransFlld:pubmed
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pubmed-article:15084179pubmed:dateRevised2008-11-21lld:pubmed
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pubmed-article:15084179pubmed:articleTitleFundamental role for HO-1 in the self-protection of renal allografts.lld:pubmed
pubmed-article:15084179pubmed:affiliationDepartment of Internal Medicine, Erasmus MC, University Medical Center Rotterdam, Rotterdam, the Netherlands. c.c.baan@erasmusmc.nllld:pubmed
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