HEMODIALYSIS-INDUCED HYPERGLYCEMIA AND ITS EFFECTS ON INFLAMMATORY CYTOKINES

这个子项目是众多研究子项目之一

This subproject is one of many research subprojects utilizing the resources provided by a Center grant funded by NIH/NCRR. The subproject and investigator (PI) may have received primary funding from another NIH source, and thus could be represented in other CRISP entries. The institution listed is for the Center, which is not necessarily the institution for the investigator. Patients with end-stage renal disease (ESRD) are at extremely high risk for cardiovascular (CV) morbidity and mortality. While some of the increased risk of CV events can be explained by traditional risk factors (such as hypertension, low HDL levels), much of the increased risk is likely associated with non-traditional risk factors. Perhaps, foremost among these is the presence of an active underlying inflammatory state as measured by elevated levels of inflammatory biomarkers such as C-reactive protein and cytokines. The etiology of this pro-inflammatory state has not been well delineated and likely derives from both features associated with the uremic state as well as features due to the dialysis procedure itself. This study aims to investigate the role of the hemodialysate solution in leading to active inflammation in ESRD patients. Non-diabetic hemodialysis patients are exposed to non-physiological levels of glucose (200 mg/dL) during each dialysis session for 3-4 hours. Experimental models have demonstrated that hyperglycemia can stimulate the production of pro-inflammatory cytokines. The aim of this study is to determine if modulating the dialysate glucose concentration can lead to reductions in pro-inflammatory cytokines (IL-6, C-reactive protein, IL-1¿ and TNF-a) and elevations in anti-inflammatory cytokines (IL-10).