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International Journal of Nephrology
Volume 2012 (2012), Article ID 608397, 11 pages
Research Article

Inflammation and Oxidative Stress in Obesity-Related Glomerulopathy

1Department of Nephrology, Shanghai East Hospital, Tongji University School of Medicine, Shanghai 200120, China
2Department of Medicine, Alpert Medical School of Brown University, Rhode Island Hospital-Middle House 301, 593 Eddy Street, Providence, RI 02903, USA

Received 2 September 2011; Accepted 6 February 2012

Academic Editor: Ayse Balat

Copyright © 2012 Jinhua Tang et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.


Obesity-related glomerulopathy is an increasing cause of end-stage renal disease. Obesity has been considered a state of chronic low-grade systemic inflammation and chronic oxidative stress. Augmented inflammation in adipose and kidney tissues promotes the progression of kidney damage in obesity. Adipose tissue, which is accumulated in obesity, is a key endocrine organ that produces multiple biologically active molecules, including leptin, adiponectin, resistin, that affect inflammation, and subsequent deregulation of cell function in renal glomeruli that leads to pathological changes. Oxidative stress is also associated with obesity-related renal diseases and may trigger the initiation or progression of renal damage in obesity. In this paper, we focus on inflammation and oxidative stress in the progression of obesity-related glomerulopathy and possible interventions to prevent kidney injury in obesity.