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. 2008 Feb;23(1):89-93.
doi: 10.3346/jkms.2008.23.1.89.

Interleukin-10 and tumor necrosis factor-alpha polymorphisms in vascular access failure in patients on hemodialysis: preliminary data in Korea

Su Ah Sung  1 , Gang Jee Ko, Sang Kyung Jo, Won Yong Cho, Hyoung Kyu Kim, So Young Lee
Affiliations

Interleukin-10 and tumor necrosis factor-alpha polymorphisms in vascular access failure in patients on hemodialysis: preliminary data in Korea

Su Ah Sung et al. J Korean Med Sci. 2008 Feb.

Abstract

Neointimal hyperplasia causes vascular stenosis and subsequent thrombosis, which result in vascular access failure in patients undergoing hemodialysis. Interleukin-10 (IL-10) and tumour necrosis factor-alpha(TNF-alpha) are involved in this inflammatory process. The aim of this study was to investigate the relationship between vascular access failure and various inflammatory markers including the genetic polymorphisms of IL-10 and TNF-alpha. Seventy-five patients on hemodialysis with an arteriovenous fistula in place or an artificial graft (18 with vascular access failure and 82 without failure) and 98 healthy individuals were genotyped for IL-10 and TNF-alpha single nucleotide polymorphisms. Clinical and laboratory data including serum IL-10 and TNF-alpha levels were compared. Stimulated IL-10 levels, from in vitro incubation of blood with lipopolysaccharide, were also obtained and compared. Female gender, hypoproteinemia, and hypertriglyceridemia were associated with vascular access failure. The basal TNF-alpha level was significantly higher in patients with access failure. The distribution of IL-10 and TNF-alpha genotype did not differ among patients with or without access failure. This study could not demonstrate a relationship between genetic polymorphisms and vascular access failure. However, an altered immune response and inflammation might contribute to vascular access failure.

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Figures

Fig. 1
Fig. 1
Comparison between percentage frequencies of interleukin-10 and tumour necrosis factor-α genotypes in healthy controls, good functioning access groups and access failure group.
Fig. 2
Fig. 2
Comparison between interleukin-10 single nucleotide polymorphisms in in vitro production of interleukin-10 protein in peripheral blood mononuclear cells after stimulating with lipopolysaccharide.
Fig. 3
Fig. 3
Comparison of the serum tumour necrosis factor-α level between the good functioning access group and the access failure group.
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