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Official Journal of the , the International Union of Phlebology and the
Indexed/Abstracted in: BIOSIS Previews, Current Contents/Clinical Medicine, EMBASE, PubMed/MEDLINE, Science Citation Index Expanded (SciSearch), Scopus
Impact Factor 0,899
Online ISSN 1827-1839
Jennifer SALUK 1, Vinod BANSAL 2, Debra HOPPENSTEADT 3, Daneyal SYED 3, Schuarazad ABRO 3, Jawed FAREED 3
1 Stritch School of Medicine, Loyola University of Chicago, Maywood, IL, USA; 2 Unit of Nephrology, Department of Internal Medicine, Loyola University Medical Center, Maywood, IL, USA; 3 Unit of Hemostasis and Thrombosis, Department of Pathology, Loyola University Medical Center, Maywood, IL, USA
BACKGROUND: As chronic kidney disease (CKD) and metabolic syndrome (MetS) share many of the same risk factors and similar inflammatory pathogenesis, multiple studies have suggested a correlation between CKD and MetS.. The purpose of this study is to investigate the prevalence of MetS in end stage renal disease (ESRD) patients. Furthermore, investigating metabolic biomarker levels in patients with ESRD may provide insight into the pathogenic processes and the development of associated comorbidities.
METHODS: Under IRB approval, plasma samples were collected from 89 patients with ESRD prior to hemodialysis. Biochips purchased from RANDOX (Co. Antrim, Northern Ireland) were used to test C peptide, ferritin, IL-6, resistin, insulin, TNFα, IL-1α, leptin, PAI-1 on 82 ESRD and 17 normal samples.
RESULTS: All biomarkers, except insulin, were significantly elevated in patients with ESRD, suggesting an ongoing inflammatory process. Patients with ESRD+MetS, as compared to ESRD-MetS, had significantly elevated leptin. Furthermore, ESRD+MetS vs. normal was significant for leptin, but ESRD-MetS vs. normal was not. ESRD+MetS and ESRD-MetS populations were not statistically different for all other biomarkers.
CONCLUSION: These findings suggest elevated Leptin in ESRD may be attributed to MetS, which is highly prevalent in the ESRD population, rather than ESRD/CKD pathogenesis alone. Lack of a significant difference for all other biomarkers suggest biomarker elevation is due to ESRD pathogenesis, rather than due to MetS as a comorbidity.