Abstract 16854: End-Stage Renal Disease Associated With Metabolic Syndrome: A Study of Biomarkers Relevant to Cardiovascular Risk

Abstract

Introduction: Metabolic syndrome (MS) represents a cluster of cardiovascular risk factors which contribute to myocardial infarction and stroke in end stage renal disease (ESRD) patients. Several metabolic biomarkers have been identified and their circulating levels provide a better understanding of the pathogenesis of MS/ESRD. The purpose of this investigation is to profile biomarkers of MS in ESRD patients. Materials and Methods: Plasma samples from 87 patients with ESRD undergoing maintenance hemodialysis and 50 normals were collected prior to a routine session. These samples were profiled for metabolic biomarkers using protein chip bioarray technology. The protein chip array was comprised of several biomarkers of MS. All results were compiled in terms of group means +/- 1 SD (SEM) and statistically analyzed. Results: In comparison to the normal samples, the ESRD group showed marked increase in circulating levels of all biomarkers. TNFa (47.4 +/- 18.3 vs 4.1 +/- 1.1 ng/mL) and IL-6 (7.8 +/- 9.1 vs 0.8 +/- 0.4 ng/mL) showed the most pronounced increase. C-peptide (14.5 +/- 4.1 vs 2.8 +/- 1.6 ng/mL), leptin (29.7 +/- 29.2 vs 5.2 +/- 7.9 ng/mL), resistan (16.1 +/- 6.0 vs 2.3 +/- 0.7 ng/mL) and ferritin (274 +/- 57 vs 57 +/- 63 ng/mL) showed a 5-fold increase in the ESRD group compared to normal. PAI-1 (5.4 +/- 5.2 vs 2.9 +/- 2.5 ng/mL), IL-1a (1.3 +/- 1.7 vs 0.35 +/- 0.07 ng/mL) and insulin (32.1 +/- 17.3 vs 17.1 +/- 1.7 ng/mL) showed modest increase in the ESRD patients. The increase in all of the MS biomarkers in the ESRD patients were highly significantly elevated, p <0.05. Conclusion: The specific biochip array for MS allows the selective determination of various biomarkers associated with this syndrome in the ESRD patients and normals. Parallel increase in resistan, insulin, C-peptide, and leptin points to the derangement of glucose metabolism in these patients. Increase IL-1a, TNFa, and ferritin suggests the upregulation of an inflammatory process. PAI-1 increase suggests a fibrinolytic deficit. The parallel derangement of the inflammatory process and metabolic syndrome contributes to the cardiovascular and cerebrovascular complications in these patients.