Mostrar el registro sencillo del ítem
dc.contributor.author | Jimenez-Sousa, Maria Angeles | |
dc.contributor.author | Fernandez-Rodriguez, Amanda | |
dc.contributor.author | Heredia, María | |
dc.contributor.author | Tamayo, Eduardo | |
dc.contributor.author | Guzman-Fulgencio, Maria | |
dc.contributor.author | Lajo, Carmen | |
dc.contributor.author | López, Elisabeth | |
dc.contributor.author | Gómez-Herreras, José I | |
dc.contributor.author | Bustamante, Jesús | |
dc.contributor.author | Bermejo-Martín, Jesús F | |
dc.contributor.author | Resino, Salvador | |
dc.date.accessioned | 2024-01-19T12:58:59Z | |
dc.date.available | 2024-01-19T12:58:59Z | |
dc.date.issued | 2012-06 | |
dc.identifier.citation | Cytokine. 2012 Jun;58(3):321-6. | es_ES |
dc.identifier.uri | http://hdl.handle.net/20.500.12105/17239 | |
dc.description.abstract | Background: Persistent inflammation and fibrosis have been related to active progression of renal deterioration and reduced survival of kidney transplant. The aim of this study was to determine the impact of single-nucleotide polymorphisms (SNPs) located in regions related to inflammatory and immune processes on the development of chronic renal allograft dysfunction (CRAD). Methods: A retrospective study was carried out on 276 patients who received kidney transplant (KT). SNPs were genotyped via the SNPlex platform. Statistical analysis was performed with SNPstat and regression logistic analyses were adjusted by age and gender of recipients and donors, cold ischemia time and the number of human leukocyte antigen (HLA) mismatches. Results: From 276 patients with KT, 118 were non-CRAD and 158 were CRAD. Three SNPs showed significant associations with CRAD development: rs1800471 in transforming growth factor beta 1 (TGFB1), rs5186 in angiotensin II receptor type 1 (AGTR1), and rs699947 in vascular endothelial growth factor A (VEGFA). GC genotype of rs1800471 was associated with increased odds of CRAD compared to GG genotype (OR=2.65 (95% confidence interval (CI)=1.09; 6.47), p=0.025), as well as AC and AA genotype of rs699947 assuming a dominant model (OR=1.80 (95% CI=1.02; 3.20), p=0.044). Besides, AC and CC genotypes of rs5186 were associated with reduced odds of CRAD assuming a dominant model (OR=0.56 (95% CI=0.33; 0.96), p=0.033). Conclusion: Our findings suggest that three genes related to immunity and inflammation (rs1800471, rs5186 and rs699947) are associated to susceptibility or protection to CRAD, and might have diagnostic utility in predicting the likelihood of developing CRAD. | es_ES |
dc.description.sponsorship | This work was supported by two Grants from Instituto de Salud Carlos III (Ref: PI08/0738 and PI11/00245) and from Junta de Castilla y León (Ref: GRS 234/A/08). MAJs, AFR and MGF are supported by Grants from Instituto de Salud Carlos III, CM10/00105, UIPY-1377/08 and CM09/00031, respectively. | es_ES |
dc.language.iso | eng | es_ES |
dc.publisher | Elsevier | es_ES |
dc.type.hasVersion | AM | es_ES |
dc.rights.uri | http://creativecommons.org/licenses/by-nc-nd/4.0/ | * |
dc.subject | Kidney transplant | es_ES |
dc.subject | Allograft rejection | es_ES |
dc.subject | SNPs | es_ES |
dc.subject | Grow factors | es_ES |
dc.subject | Biomarkers | es_ES |
dc.subject.mesh | Kidney Transplantation | es_ES |
dc.subject.mesh | Polymorphism, Single Nucleotide | es_ES |
dc.subject.mesh | Adult | es_ES |
dc.subject.mesh | Aged | es_ES |
dc.subject.mesh | Female | es_ES |
dc.subject.mesh | Graft Rejection | es_ES |
dc.subject.mesh | Humans | es_ES |
dc.subject.mesh | Male | es_ES |
dc.subject.mesh | Middle Aged | es_ES |
dc.subject.mesh | Receptor, Angiotensin, Type 1 | es_ES |
dc.subject.mesh | Retrospective Studies | es_ES |
dc.subject.mesh | Transforming Growth Factor beta1 | es_ES |
dc.subject.mesh | Transplantation, Homologous | es_ES |
dc.subject.mesh | Vascular Endothelial Growth Factor A | es_ES |
dc.title | Genetic polymorphisms located in TGFB1, AGTR1, and VEGFA genes are associated to chronic renal allograft dysfunction | es_ES |
dc.type | research article | es_ES |
dc.rights.license | Attribution-NonCommercial-NoDerivatives 4.0 Internacional | * |
dc.identifier.pubmedID | 22433249 | es_ES |
dc.format.volume | 58 | es_ES |
dc.format.number | 3 | es_ES |
dc.format.page | 321-326 | es_ES |
dc.identifier.doi | 10.1016/j.cyto.2012.02.017 | es_ES |
dc.contributor.funder | Instituto de Salud Carlos III | es_ES |
dc.contributor.funder | Junta de Castilla y León (España) | es_ES |
dc.description.peerreviewed | Sí | es_ES |
dc.identifier.e-issn | 1096-0023 | es_ES |
dc.relation.publisherversion | https://doi.org/10.1016/j.cyto.2012.02.017 | es_ES |
dc.identifier.journal | Cytokine | es_ES |
dc.repisalud.centro | ISCIII::Centro Nacional de Microbiología | es_ES |
dc.repisalud.institucion | ISCIII | es_ES |
dc.rights.accessRights | open access | es_ES |
dc.relation.projectFECYT | info:eu-repo/grantAgreement/MICINN//PI11%2F00245/ES/Erradicación del VHC en pacientes coinfectados por VIH%2FVHC: efectos sobre la inflamación, el daño endotelial, la activación inmune y la aterosclerosis preclínica/ | es_ES |
dc.relation.projectFECYT | info:eu-repo/grantAgreement/MICINN//CM10%2F00105/ES/CM10%2F00105/ | es_ES |
dc.relation.projectFECYT | info:eu-repo/grantAgreement/MICINN//CM09%2F00031/ES/CM09%2F00031/ | es_ES |
dc.relation.projectFIS | info:eu-repo/grantAgreement/ES/PI08/0738 | es_ES |
dc.relation.projectFIS | info:eu-repo/grantAgreement/ES/UIPY-1377/08 | es_ES |