Metabolic syndrome, characterized by truncal obesity, hypertriglyceridemia, elevated blood pressure, and insulin resistance, is recognized increasingly as a major risk factor for kidney disease and also is a common feature of patients who are on dialysis. Obesity is considered a major generator of metabolic syndrome. Early in the course of obesity-initiated metabolic syndrome, structural and functional changes similar to diabetic kidney disease occur. Previous studies examined the histologic and functional changes that occur in the kidney in the early stages of obesity caused by a high-fat diet. They reported that a high-fat diet caused increased arterial pressure, hyperinsulinemia, activation of the renin-angiotensin system, glomerular hyperfiltration, and structural changes in the kidney that may be the precursors of more severe glomerular injury associated with prolonged obesity. Among several factors causing renal injury, Rho-kinase also plays an important role in the pathogenesis of obesity-related renal disease. We further propose that perinephric adipose tissues could be a source of inflammatory chemokines, which acts in concert with the renal Rho-kinase stimulated in situ to exacerbate renal inflammation. In this review, we note the mechanisms inducing chronic kidney disease (CKD) by obesity, especially the relation between insulin resistance and CKD.