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

• Published in: European journal of inflammation Vol. 7; no. 3; pp. 191 - 194
• Main Authors: Balistreri, C.R., Vecchi, M. Li, Iatrino, R., Caruso, M., Incalcaterra, E., Caruso, C., Candore, G.
• Format: Journal Article
• Language: English
• Published: London, England SAGE Publications 01-09-2009; SAGE PUBLICATIONS, INC; SAGE Publishing
• Subjects: Genotype & phenotype; Health risk assessment; Kidney diseases; Polymorphism; CVD; CCR5; inflammation; CKD; TLR4
• ISSN: 2058-7392; 1721-727X; 2058-7392
• DOI: 10.1177/1721727X0900700310

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.