Obesity is a major risk factor for renal disease and can cause de novo glomerulopathy. The characteristic finding of obesity-induced renal injury includes glomerular hypertrophy, glomerular basement membrane thickening, mesangial matrix expansion, and increased renal inflammation. These changes may lead to albuminuria, a progressive impairment of renal function, glomerulosclerosis and tubulointerstitial fibrosis. The mechanisms of obesity-related glomerulopathy (ORG) are not well understood however, several mechanisms acting singly or in combination have been suggested as excess excretory load, excess renal sodium retention and insulin resistance (IR) and hyperinsulinemia, increased monocyte chemoattractant protein 1 (MCP-1) expression, Lipotoxicity in proximal tubular cells, increased inflammatory cytokine production such as Interleukin (IL) IL-6, IL-1, and tumor necrosis factor (TNF-α). Activation of NFκB transcription, increase Leptin levels, reduction in plasma adiponectin expression with its anti-inflammatory effects, decrease nitric oxide (NO) level, increase reactive oxygen species (ROS) generation, Hyperlipidemia, and increases in plasma renin activity, angiotensinogen, angiotensin-converting enzyme activity, and circulating AngII. Many lines of treatment are suggested for ORG as Peroxisome proliferator-activated receptors (PPAR) Agonistic, Statins, anti-inflammatory therapy, and antioxidants are under trial. Weight loss decreases of proinflammatory factors, increase of anti-inflammatory molecules and reduces oxidative stress state in obesity, which may protect renal function. This review discusses recent data about ORG, the characteristics of pathogens and possible interventions to prevent kidney injury in obesity.