| dc.description.abstract | 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. Chronic hemodialysis, typically accompanied by oxidative stress and inflammation, may be also associated with replicative senescence. To test this hypothesis, we determined telomere length and telomerase activity in peripheral blood mononuclear cells (PBMCs) in a cross-sectional study. Hemodialysis patients at the University Hospital Larissa and healthy controls were studied. Telomere length was determined by the TeloTAGGG Telomere Length Assay and telomerase activity by Telomerase PCR-ELISA (Roche Diagnostics GmbH, Mannheim, Germany). We enrolled 43 hemodialysis patients (17 females; age 65.0 +/- 12.7 years) and 23 controls (six females; age 62.1 +/- 15.7 years). Between the two groups, there was no difference in telomere length (6.95 +/- 3.25 vs. 7.31 +/- 1.96kb; P=0.244) or in telomerase activity (1.82 +/- 2.91 vs. 2.71 +/- 3.0; P=0.085). Telomere length correlated inversely with vintage of hemodialysis (r=-0.332, P=0.030). In hemodialysis patients, positive telomerase activity correlated with telomere length (r=0.443, P=0.030). Only age, and neither telomere length nor telomerase activity, was an independent survival predictor (hazard ratio 1.116, 95% confidence interval 1.009-1.234, P=0.033). In this study, telomere length and telomerase activity in PBMCs are not altered in hemodialysis patients compared with healthy controls. Long duration of hemodialysis treatment is associated with telomere shortening and positive telomerase activity with an increased telomere length in PBMCs of hemodialysis patients. The underlying mechanism and clinical implications of our findings require further investigation. | en |