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Baan, C. et al.

Baan, Peeters, Lemos, Uitterlinden, Doxiadis, Claas, Ijzermans, Roodnat, Weimar,

Fundamental role for HO-1 in the self-protection of renal allografts.

Tissue 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.[1]

References

Fundamental role for HO-1 in the self-protection of renal allografts. Baan, C., Peeters, A., Lemos, F., Uitterlinden, A., Doxiadis, I., Claas, F., Ijzermans, J., Roodnat, J., Weimar, W. American journal of transplantation : official journal of the American Society of Transplantation and the American Society of Transplant Surgeons. (2004) [Pubmed]

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