NDT Advance Access originally published online on February 10, 2009
Nephrology Dialysis Transplantation 2009 24(5):1384-1387; doi:10.1093/ndt/gfp038
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© The Author [2009]. Published by Oxford University Press on behalf of ERA-EDTA. All rights reserved. For Permissions, please e-mail: journals.permissions@oxfordjournals.org
Systemic inflammation, metabolic syndrome and progressive renal disease
1 Division of Nephrology, Hypertension and Transplantation, Department of Medicine, University of Florida, Gainesville, FL 32610, USA 2 Division of Nephrology, Dialysis and Transplantation, Department of Biomedical Sciences, University of Foggia, Foggia, Italy 3 Department of Nephrology, Monash Medical Centre, Clayton, VIC 3168, Australia 4 Department of Nephrology, Ewha Womans University School of Medicine, Seoul, Korea 5 Division of Renal Diseases and Hypertension, University of Colorado, Aurora, CO 80045, USA
Correspondence and offprint requests to: Pietro Cirillo, Division of Nephrology, Dialysis and Transplantation, Department of Biomedical Sciences, University of Foggia, College of Medicine, Viale L. Pinto 1, 71100, Foggia, Italy. Tel: +39-0881-732054; Fax: +39-0881-736001; E-mail: p.cirillo@unifg.it
Keywords: fructose; metabolic syndrome; monocyte chemoattractant protein-1; uric acid
| The first 150 words of the full text of this article appear below. |
| Introduction |
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Systemic inflammation is a characteristic feature of metabolic syndrome and cardiovascular (CV) disease. One common marker used to define systemic inflammation is the plasma level of C-reactive protein (CRP) [1]. Studies by Ridker et al. have shown that subjects with elevated plasma CRP levels have an increased risk for CV death [2,3]. More recent studies have shown that an elevated CRP level may also increase the risk for CV events in patients with chronic kidney disease (CKD) [4]. Furthermore, an elevation in CRP also increases the risk for progression of kidney disease in subjects with CKD [5]. In addition, a number of therapeutic agents such as aspirin [6], statins [7,8], angiotensin converting enzyme (ACE) inhibitors [9] and antioxidants [10] have been reported to both reduce CRP levels and improve CV outcomes, thereby suggesting that
| Mechanisms responsible for the systemic inflammatory response in subjects with metabolic syndrome |
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| Fructose as a means for inducing systemic inflammation and renal damage progression |
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| Uric acid, MCP-1 expression, and renal progression |
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| Summary |
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