TY - JOUR
T1 - Interleukin-10 and tumor necrosis factor-α polymorphisms in vascular access failure in patients on hemodialysis
T2 - Preliminary data in Korea
AU - Su, Ah Sung
AU - Gang, Jee Ko
AU - Sang, Kyung Jo
AU - Won, Yong Cho
AU - Hyoung, Kyu Kim
AU - So, Young Lee
N1 - Copyright:
Copyright 2008 Elsevier B.V., All rights reserved.
PY - 2008/2
Y1 - 2008/2
N2 - 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.
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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U2 - 10.3346/jkms.2008.23.1.89
DO - 10.3346/jkms.2008.23.1.89
M3 - Article
C2 - 18303205
AN - SCOPUS:40549092667
VL - 23
SP - 89
EP - 93
JO - Journal of Korean Medical Science
JF - Journal of Korean Medical Science
SN - 1011-8934
IS - 1
ER -