Chronic Kidney Disease and Inflammation: Role of +896A/G Pro-Inflammatory Polymorphism of TLR4 Gene and Δ32 Deletion of CCR5 Gene

Chronic inflammation seems implicated in the pathophysiology of chronic kidney diseases (CKD) and the development of its complications, such as cardiovascular diseases (CVD). Genes encoding inflammatory molecules are, hence, good candidates for CVD risk in haemodialysis patients (HD). We therefore e...

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Main Authors: C.R. Balistreri PhD., M. Li Vecchi, R. Iatrino, M. Caruso, E. Incalcaterra, C. Caruso, G. Candore
Format: Article
Language:English
Published: SAGE Publishing 2009-09-01
Series:European Journal of Inflammation
Online Access:https://doi.org/10.1177/1721727X0900700310
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author C.R. Balistreri PhD.
M. Li Vecchi
R. Iatrino
M. Caruso
E. Incalcaterra
C. Caruso
G. Candore
author_facet C.R. Balistreri PhD.
M. Li Vecchi
R. Iatrino
M. Caruso
E. Incalcaterra
C. Caruso
G. Candore
author_sort C.R. Balistreri PhD.
collection DOAJ
description Chronic inflammation seems implicated in the pathophysiology of chronic kidney diseases (CKD) and the development of its complications, such as cardiovascular diseases (CVD). Genes encoding inflammatory molecules are, hence, good candidates for CVD risk in haemodialysis patients (HD). We therefore evaluated whether +896A/G TLR4 polymorphism and CCR5A32 deletion are risk factors for CKD and CVD. We examined the two gene variants in 72 HD patients and in 125 controls from Sicily. No significant differences in the genotype distribution and allele frequencies of the two gene variants were observed between patients and controls. The same results were obtained by analysing the combined effect of the two proinflammatory (+896ATLR4 and wt CCR5) alleles. However, the high responder proinflammatory (+896A+TLR4/wt+CCR5) genotype seems to be a possible independent risk factor for CVD development in HD patients. Our results suggest that HD patients with a high responder pro-inflammatory genotype have an increase CVD risk.
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spelling doaj.art-be0df92395284e9b8e6a69605111af562022-12-21T22:46:02ZengSAGE PublishingEuropean Journal of Inflammation1721-727X2009-09-01710.1177/1721727X0900700310Chronic Kidney Disease and Inflammation: Role of +896A/G Pro-Inflammatory Polymorphism of TLR4 Gene and Δ32 Deletion of CCR5 GeneC.R. Balistreri PhD.0M. Li Vecchi1R. Iatrino2M. Caruso3E. Incalcaterra4C. Caruso5G. Candore6Gruppo di Studio sull'Immunosenescenza, Dipartimento di Biopatologia e Metodologie Biomediche, Università di Palermo, PalermoDipartimento di Medicina Interna, Malattie Cardiovascolari e Nefro-Urologiche, Università di Palermo, Palermo, ItalyDipartimento di Medicina Interna, Malattie Cardiovascolari e Nefro-Urologiche, Università di Palermo, Palermo, ItalyDipartimento di Medicina Interna, Malattie Cardiovascolari e Nefro-Urologiche, Università di Palermo, Palermo, ItalyDipartimento di Medicina Interna, Malattie Cardiovascolari e Nefro-Urologiche, Università di Palermo, Palermo, ItalyGruppo di Studio sull'Immunosenescenza, Dipartimento di Biopatologia e Metodologie Biomediche, Università di Palermo, PalermoGruppo di Studio sull'Immunosenescenza, Dipartimento di Biopatologia e Metodologie Biomediche, Università di Palermo, PalermoChronic inflammation seems implicated in the pathophysiology of chronic kidney diseases (CKD) and the development of its complications, such as cardiovascular diseases (CVD). Genes encoding inflammatory molecules are, hence, good candidates for CVD risk in haemodialysis patients (HD). We therefore evaluated whether +896A/G TLR4 polymorphism and CCR5A32 deletion are risk factors for CKD and CVD. We examined the two gene variants in 72 HD patients and in 125 controls from Sicily. No significant differences in the genotype distribution and allele frequencies of the two gene variants were observed between patients and controls. The same results were obtained by analysing the combined effect of the two proinflammatory (+896ATLR4 and wt CCR5) alleles. However, the high responder proinflammatory (+896A+TLR4/wt+CCR5) genotype seems to be a possible independent risk factor for CVD development in HD patients. Our results suggest that HD patients with a high responder pro-inflammatory genotype have an increase CVD risk.https://doi.org/10.1177/1721727X0900700310
spellingShingle C.R. Balistreri PhD.
M. Li Vecchi
R. Iatrino
M. Caruso
E. Incalcaterra
C. Caruso
G. Candore
Chronic Kidney Disease and Inflammation: Role of +896A/G Pro-Inflammatory Polymorphism of TLR4 Gene and Δ32 Deletion of CCR5 Gene
European Journal of Inflammation
title Chronic Kidney Disease and Inflammation: Role of +896A/G Pro-Inflammatory Polymorphism of TLR4 Gene and Δ32 Deletion of CCR5 Gene
title_full Chronic Kidney Disease and Inflammation: Role of +896A/G Pro-Inflammatory Polymorphism of TLR4 Gene and Δ32 Deletion of CCR5 Gene
title_fullStr Chronic Kidney Disease and Inflammation: Role of +896A/G Pro-Inflammatory Polymorphism of TLR4 Gene and Δ32 Deletion of CCR5 Gene
title_full_unstemmed Chronic Kidney Disease and Inflammation: Role of +896A/G Pro-Inflammatory Polymorphism of TLR4 Gene and Δ32 Deletion of CCR5 Gene
title_short Chronic Kidney Disease and Inflammation: Role of +896A/G Pro-Inflammatory Polymorphism of TLR4 Gene and Δ32 Deletion of CCR5 Gene
title_sort chronic kidney disease and inflammation role of 896a g pro inflammatory polymorphism of tlr4 gene and δ32 deletion of ccr5 gene
url https://doi.org/10.1177/1721727X0900700310
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