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

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-α (TNF-α) 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-α. 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-α single nucleotide polymorphisms. Clinical and laboratory data including serum IL-10 and TNF-α 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-α level was significantly higher in patients with access failure. The distribution of IL-10 and TNF-α 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.