Interleukin Variants Are Associated with the Development and Progression of IgA Nephropathy: A Candidate-Gene Association Study and Meta-Analysis.

The interleukin-1 gene cluster encodes cytokines, which modulate mesangial cell proliferation and matrix expansion, both constituting central factors in the development and progression of immunoglobulin A nephropathy (IgAN). A candidate-gene study was performed to examine the association of polymorphisms of the interleukin-1 gene cluster with the risk of progressive IgAN. To gain deeper insights into the involvement of interleukin genes in IgAN, a meta-analysis of genetic association studies (GAS) that examine the association between interleukin variants and IgAN was conducted.

Tumor Necrosis Factor-α G-308A Polymorphism and Sporadic IgA Nephropathy: A Meta-Analysis Using a Genetic Model-Free Approach.

Tumor necrosis factor-α (TNF-α) is a potent pro-inflammatory cytokine, involved in the pathogenesis and progression of immunoglobulin A nephropathy (IgAN). A bi-allelic polymorphism in the promoter region, at position -308 (G/A) of the - gene (rs1800629) is associated with an increased TNF-a production. However, several previous association studies of - G-308A polymorphism and IgAN rendered contradictory findings.

Telomere Length in Peripheral Blood Mononuclear Cells of Patients on Chronic Hemodialysis Is Related With Telomerase Activity and Treatment Duration.

Telomere shortening to a critical limit is associated with replicative senescence. This process is prevented by the enzyme telomerase. Oxidative stress and chronic inflammation are factors accelerating telomere loss.

Effect of endothelin-1 on the transmesothelial resistance of isolated visceral sheep peritoneum.

The mesothelium is part of the peritoneal barrier that manages the water and ion transport essential for peritoneal dialysis (PD) treatment. In addition, it has a central role in the pathogenesis of peritoneal fibrosis and the resulting ultrafiltration failure observed in many PD patients. Endothelin-1 (ET-1) is a potent vasoactive peptide originally described as an endothelial cell-derived factor In addition, ET-1 has been shown to stimulate fibrogenic activity in various organs by regulating the production and turnover of matrix components.