Abstract 501: Up-Regulation of Inflammatory Mediators and Markers of Metabolic Deraignment in ESRD as Studied by Biochip Array Analysis
Introduction: End stage renal disease represents a complex syndrome with multiple pathophysiological processes involving vascular, inflammatory, thrombotic, and metabolic deraignment. To understand the pathophysiology of this complex syndrome, profiling of mediators of inflammation and metabolic deraignment provides a unique approach. This study was designed to utilize biochip array technology to compare the biomarker profiles of a maintenance hemodialysis cohort (n=81) with healthy normal male and female volunteers (n=41).
Materials and Methods: Blood samples from the ESRD group were collected prior to the hemodialysis, centrifuged immediately, and frozen at -80 degrees Celsius. The normal samples represented citrated plasmas from 41 healthy individuals, which were processed in an identical manner as the ESRD group. High sensitivity inflammatory cytokine chips to profile IL-2, IL-4, IL-6, IL-8, IL-10, VEGF, IFN-gamma, IL1-alpha, IL1-beta, MCP1, and EGF and metabolic array chip to analyze C-Peptide, ferritin, resistin, insulin, leptin, and PAI-1 were used employing Evidence Investigator (Randox, UK).
Results: In the inflammatory biochip array analysis, except for IL-2 and EGF, all the inflammatory biomarkers were found to be significantly higher than the normal group (p<0.0001). The ESRD group exhibited marked variations in the circulating levels of the inflammatory mediators and the extent of increase also varied. In the metabolic chip array analysis, all of the markers of metabolic deraignment were significantly increased, except insulin, where a trend towards increased levels was noted.
Conclusions: These results clearly demonstrate the complexity of the pathophysiologic event in ESRD patients. A widespread increase in the inflammatory mediators, coupled with the higher levels of metabolic deraignment markers suggest that the ESRD patients not only have an ongoing inflammatory process but also sustain metabolic deraignment as evident by the results obtained by the metabolic array chip. Profiling of these mediators not only provides an understanding of the pathogenesis of this condition, but may be helpful in the risk stratification and clinical management of these patients.
Author Disclosures: V. Bansal: None. D. Syed: None. D. Hoppensteadt: None. J. Fareed: None.
- © 2014 by American Heart Association, Inc.