Jimenez-Sousa, Maria AngelesLópez, ElisabethFernandez-Rodriguez, AmandaTamayo, EduardoFernandez-Navarro, Pablo LSegura-Roda, LauraHeredia, MaríaGómez-Herreras, José IBustamante, JesúsGarcía-Gómez, Juan MiguelBermejo-Martin, Jesús FResino, Salvador2019-02-012019-02-012012-07-20BMC Med Genet. 2012 Jul 20;13:58.1471-2350http://hdl.handle.net/20.500.12105/7065BACKGROUND: Chronic kidney disease progression has been linked to pro-inflammatory cytokines and markers of inflammation. These markers are also elevated in end-stage renal disease (ESRD), which constitutes a serious public health problem. OBJECTIVE: To investigate whether single nucleotide polymorphisms (SNPs) located in genes related to immune and inflammatory processes, could be associated with ESRD development. DESIGN AND METHODS: A retrospective case-control study was carried out on 276 patients with ESRD and 288 control subjects. Forty-eight SNPs were genotyped via SNPlex platform. Logistic regression was used to assess the relationship between each sigle polymorphism and the development of ESRD. RESULTS: Four polymorphisms showed association with ESRD: rs1801275 in the interleukin 4 receptor (IL4R) gene (OR: 0.66 (95%CI = 0.46-0.95); p = 0.025; overdominant model), rs4586 in chemokine (C-C motif) ligand 2 (CCL2) gene (OR: 0.70 (95%CI = 0.54-0.90); p = 0.005; additive model), rs301640 located in an intergenic binding site for signal transducer and activator of transcription 4 (STAT4) (OR: 1.82 (95%CI = 1.17-2.83); p = 0.006; additive model) and rs7830 in the nitric oxide synthase 3 (NOS3) gene (OR: 1.31 (95%CI = 1.01-1.71); p = 0.043; additive model). After adjusting for multiple testing, results lost significance. CONCLUSION: Our preliminary data suggest that four genetic polymorphisms located in genes related to inflammation and immune processes could help to predict the risk of developing ESRD.engVoRhttp://creativecommons.org/licenses/by/4.0/AgedCase-Control StudiesChemokine CCL2FemaleGenetic Predisposition to DiseaseGenotypeHumansImmune SystemInflammationKidney Failure, ChronicMaleMiddle AgedModels, GeneticNitric Oxide Synthase Type IIIReceptors, Interleukin-4Regression AnalysisRetrospective StudiesSTAT4 Transcription FactorPolymorphism, GeneticAtribución 4.0 Internacional228175301315810.1186/1471-2350-13-58BMC medical geneticsopen access