A419C (E111A) Polymorphism of the Glyoxalase I Gene and Vascular Complications in Chronic Hemodialysis Patients
Advanced glycation end products (AGEs) take part in the pathogenesis of vascular, diabetic, and uremic complications. Their precursors are detoxified by the glyoxalase system. Our aim was to study A419C (E111A) single nucleotide polymorphism (SNP) of the glyoxalase I gene in hemodialysis (HD) patien...
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Published in | Annals of the New York Academy of Sciences Vol. 1126; no. 1; pp. 268 - 271 |
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Main Authors | , , , , , |
Format | Journal Article |
Language | English |
Published |
Malden, USA
Blackwell Publishing Inc
01.04.2008
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Subjects | |
Online Access | Get full text |
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Summary: | Advanced glycation end products (AGEs) take part in the pathogenesis of vascular, diabetic, and uremic complications. Their precursors are detoxified by the glyoxalase system. Our aim was to study A419C (E111A) single nucleotide polymorphism (SNP) of the glyoxalase I gene in hemodialysis (HD) patients. A419C SNP, several laboratory parameters including soluble receptor for AGEs (sRAGE), and clinical data were studied in 214 HD patients and 89 controls. Allelic and genotypic frequencies did not differ between HD patients and controls. A419C SNP was significantly linked with serum sRAGE, which sensitively reflects the AGE burden of the organism (3986 ± 1638 pg/mL in the CC variant versus 3277 ± 1398 pg/mL in the AC variant and 3297 ± 1445 pg/mL in the AA variant, P < 0.01). In the CC variant, significantly higher prevalence of cardiovascular disease and peripheral vascular disease was found, while the prevalence of hypertension, diabetes mellitus, and dyslipidemia did not differ between genotypes. In summary, in this study we demonstrate for the first time the association of A419C polymorphism of the glyoxalase I gene with sRAGE levels and show the genetic predisposition to vascular complications in HD patients. |
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Bibliography: | ArticleID:NYAS1433012 ark:/67375/WNG-8803R895-N istex:91094BFCD7EC52555A3E7354ADB92258EC3CD7D1 ObjectType-Article-1 SourceType-Scholarly Journals-1 ObjectType-Feature-2 content type line 23 |
ISSN: | 0077-8923 1749-6632 1930-6547 |
DOI: | 10.1196/annals.1433.012 |