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

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 lipopolysaccharicle, 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 an inflammation might contribute to vascular access failure.