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Role of cytokines in the pathogenesis of acute and chronic kidney disease, glomerulonephritis, and end-stage kidney disease

Authors Ortega L, Fornoni A

Published 14 May 2010 Volume 2010:2 Pages 49—62

DOI https://doi.org/10.2147/IJICMR.S10111

Review by Single-blind

Peer reviewer comments 2


Luis M Ortega, Alessia Fornoni

Division of Nephrology and Hypertension, Department of Medicine, Miller School of Medicine, University of Miami, Miami, FL, USA

Abstract: Cytokines are soluble mediators that are released from sites of local injury exposed to an inflammatory environment. In kidney diseases, cytokines can be released by circulating leukocytes and/or from activated or injured kidney cells, which in turn attract and activate leukocytes to specific sites of injury. Therefore, cytokines may act in a systemic, paracrine, or an autocrine fashion. Different patterns of pro-inflammatory and anti-inflammatory cytokines expression and activation characterize acute kidney injury (AKI), glomerulonephritis (GMN), and end-stage kidney disease (ESKD). Moreover, plasma levels of certain cytokines and gene polymorphisms for certain cytokines may have predictive value in these different clinical scenarios. The present review will compile information regarding the role of different types of cytokines in the pathogenesis of AKI, GMN, and ESKD. Both clinical data and experimental models of injury will be discussed.

Keywords: cytokines, acute kidney injury, glomerulonephritis, hemodialysis, peritoneal dialysis, end-stage kidney disease, inflammation

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