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. 1. Introduction Obesity has become a heavy public health problem in the United States, with a prevalence among adults increasing to 32% from 13% between the 1960s and 2004 [1]. Currently, 66% of adults and 16% of children and adolescents are overweight or obese [1]. Although obesity has long been recognized as an independent risk factor for cardiovascular diseases and diabetes mellitus, newer research points to obesity as an important risk factor for chronic kidney diseases (CKDs) [2–4]. In 1974, Weisinger et al. [5] firstly reported that massive obese patients developed nephrotic-range proteinuria. Subsequent studies confirmed that obesity could induce renal injury, namely, obesity-related glomerulopathy (ORG) [6–8]. A large-scale clinicopathologic study including 6818 renal biopsies from 1986 to 2000 revealed a progressive increase in biopsy incidence of ORG from 0.2% in 1986–1990 to 2.0% in 1996–2000 [8]. The tenfold increase in incidence of ORG over 15 years suggests a newly emerging epidemic [8]. The clinical characteristics of subjects with ORG typically manifest with nephrotic or subnephrotic proteinuria, accompanied by renal insufficiency [8–10]. Histologically, ORG presents as focal segmental glomerulosclerosis (FSGS) and glomerular hypertrophy or glomerular hypertrophy alone and relatively decreased podocyte density and number and mild foot process fusion [8, 11, 12]. Clinically, it is distinguished from idiopathic FSGS (I-FSGS) by its lower incidence of nephrotic syndrome, more benign course, and slower progression of proteinuria and renal failure [8, 11]. ORG is an increasing cause of end-stage renal disease (ESRD). The pathophysiology of ORG
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