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

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

Research output: Contribution to journalArticle

12 Citations (Scopus)

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-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.

Original languageEnglish
Pages (from-to)89-93
Number of pages5
JournalJournal of Korean Medical Science
Volume23
Issue number1
DOIs
Publication statusPublished - 2008 Feb 1

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Korea
Interleukin-10
Blood Vessels
Renal Dialysis
Tumor Necrosis Factor-alpha
Genetic Polymorphisms
Hypoproteinemia
Hypertriglyceridemia
Arteriovenous Fistula
Hyperplasia
Single Nucleotide Polymorphism
Lipopolysaccharides
Pathologic Constriction
Thrombosis
Genotype
Inflammation
Transplants
Serum

Keywords

  • Arteriovenous shunt, surgical
  • Constriction, pathologic
  • Polymorphism, single nucleotide
  • Renal dialysis

ASJC Scopus subject areas

  • Medicine(all)

Cite this

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title = "Interleukin-10 and tumor necrosis factor-α 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-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.",
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T2 - Preliminary data in Korea

AU - Su, Ah Sung

AU - Ko, Gang Jee

AU - Jo, Sang Kyung

AU - Cho, Won Yong

AU - Hyoung, Kyu Kim

AU - So, Young Lee

PY - 2008/2/1

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AB - 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.

KW - Arteriovenous shunt, surgical

KW - Constriction, pathologic

KW - Polymorphism, single nucleotide

KW - Renal dialysis

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