Role of non-HLA genetic variants in end-stage renal disease

Cytokines and intercellular adhesion molecule (ICAM) play a crucial role in the pathogenesis of primary kidney disease and progression to end‐stage renal disease (ESRD). Cytokine secretion is reported to be dependent on the single nucleotide polymorphisms located in the cytokine genes. The role of d...

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Bibliographic Details
Published in:Tissue antigens 2009-08, Vol.74 (2), p.147-155
Main Authors: Ranganath, P., Tripathi, G., Sharma, R. K., Sankhwar, S. N., Agrawal, S.
Format: Article
Language:English
Subjects:
Adult
Case-Control Studies
Cell adhesion molecules
Cytokines
Cytokines - genetics
End-stage renal disease
Female
Gene Frequency
Gene polymorphism
Genetic Linkage
Genotype
HLA Antigens - genetics
Humans
inflammation
intercellular adhesion molecule 1
Intercellular Adhesion Molecule-1 - genetics
intercellular adhesive molecules
Interleukin 4
Interleukin 6
Interleukin-4 - genetics
Interleukin-6 - genetics
Kidney diseases
Kidney Failure, Chronic - genetics
Male
Middle Aged
Neural Cell Adhesion Molecules - genetics
Polymorphism, Single Nucleotide - physiology
Risk factors
single nucleotide polymorphisms
Single-nucleotide polymorphism
Statistical analysis
Tumor necrosis factor-a
Tumor Necrosis Factor-alpha - genetics
Young Adult
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Summary:Cytokines and intercellular adhesion molecule (ICAM) play a crucial role in the pathogenesis of primary kidney disease and progression to end‐stage renal disease (ESRD). Cytokine secretion is reported to be dependent on the single nucleotide polymorphisms located in the cytokine genes. The role of different polymorphisms in cytokines and ICAM genes as probable susceptibility factors for ESRD has been explored in the present study. The study was conducted on 258 ESRD patients and on ethnically matched 569 controls. Individuals were genotyped for interleukin (IL)‐6 (G174C), IL‐4 (C590T), tumor necrosis factor‐α (TNF‐α) (−G308A and −G238A) and ICAM‐1 (A469G) gene polymorphisms using standard polymerase chain reaction–restriction fragment length polymorphism–based method. We observed significant difference in the genotype frequencies of the TNF‐α−308AA [P = 0.001; odds ratios (OR) = 7.61, 95% confidence intervals (CI) = 2.1–27.9] and TNF‐α−238AA (P = 0.001; OR = 5.8, 95% CI = 2.2–15.1). Furthermore, C allele of IL‐6 −G174C and G allele of ICAM‐1 A469G were significantly different in ESRD patients when compared with controls (P = 0.0001; OR = 5.5, 95% CI = 3.9–7.7 and P 
ISSN:0001-2815
1399-0039
DOI:10.1111/j.1399-0039.2009.01276.x