Obesity is the major risk factor for type 2 diabetes, which in turn is associated with nephropathy in about one third of patients. Obesity is also an independent risk factor for chronic renal disease, regardless of the association with diabetes. Furthermore, chronic renal disease is the strongest risk factor for cardiovascular morbidity and mortality in people with diabetes and without. However, the mechanisms responsible for the adverse nephrologic effects of obesity and type 2 diabetes are not clear, but likely involve insulin resistance, low-grade systemic inflammation, hyperlipidemia, and increased synthesis of vasoactive and fibrogenic substances, including angiotensin II, insulin, leptin and transforming growth factor β1. These substances may individually or interactively affect glomerular hyperfiltration, renal venous pressure, mesangial cell hypertrophy and matrix production, ultimately leading to renal scarring, impaired glomerular filtration rate, micro- and macro- albuminuria and end-stage renal disease (ESDR). Of interest, the risk for glomerular hyperfiltration and hyperperfusion is enhanced especially in subjects with abdominal obesity. Both conditions predispose to microalbuminuria, an early marker of renal disease and increased cardiovascular risk.