title: Polymorphisms in IFN-γ, TNF-α and IL-10 in patients on maintenance haemodialysis.
abstract: The dysbalance in the expression of proinflammatory and anti-inflammatory cytokines, which is partially genetically determined, might have essential impact on the clinical outcome and survival of haemodialysed (HD) patients. A total of 500 HD patients and 500 healthy controls were genotyped for three single-nucleotide polymorphisms (SNPs: TNFA -308G/A, IL10 -1082G/A, IFNG +874A/T). To detect the SNPs' impact on clinical outcome and survival, the HD population was divided into two subgroups depending on the length of HD therapy. The genotypes and phenotypes were correlated with two years followed up laboratory parameters and survival of HD patients. The one-year HD departed patients exhibited significantly higher age (P = 0.0167), C-reactive protein (P = 0.0012), lower nutritional (body mass index, P = 0.0168; dry weight, P = 0.0207; albumin, P = 0.005; triglycerides, P = 0.0174), haematological (red blood cells count, P = 0.0210; haemoglobin, P = 0.0159; haematocrit, P = 0.0368) and HD efficacy parameters (Kt/V, P = 0.0273) compared to long-term HD survivors. Both HD and control population showed similar genotype distribution except for higher occurrence of TNFA A/A homozygotes in healthy controls (P = 0.008). There were no differences in both genotypes and phenotypes in HD subgroups because of the low number of patients in one- -year HD departed patients. Neither genotype nor phenotype had an impact on patients' survival. From our results we cannot infer that the promoter region SNPs of immune system response-regulating cytokines IL-10, TNF-α and IFN-γ have a major impact on clinical outcome of patients on maintenance haemodialysis.
authors: Institute for Clinical and Experimental Medicine, Department of Nephrology, Prague, Czech Republic. sibl@medicon.cz
authors: S
authors: S
authors: Bloudíčková
authors: L
authors: L
authors: Kuthanová
authors: J A
authors: JA
authors: Hubáček
mesh_terms: D000368:Aged; D002097:C-Reactive Protein / Q000032:analysis / Q000378:metabolism; D015331:Cohort Studies; D005260:Female; D005838:Genotype; D006801:Humans; D007371:Interferon-gamma / Q000235:genetics*; D016753:Interleukin-10 / Q000235:genetics*; D007676:Kidney Failure, Chronic / Q000453:epidemiology / Q000235:genetics* / Q000628:therapy*; D008297:Male; D008875:Middle Aged; D015596:Nutrition Assessment; D020641:Polymorphism, Single Nucleotide; D011446:Prospective Studies; D006435:Renal Dialysis; D016896:Treatment Outcome; D014409:Tumor Necrosis Factor-alpha / Q000235:genetics*
chemical_list: D014409:Tumor Necrosis Factor-alpha; D016753:Interleukin-10; D007371:Interferon-gamma; D002097:C-Reactive Protein