Cilostazol, a specific inhibitor of phosphodiesterase 3, can prevent platelet aggregation and dilate blood vessels via an increase in cyclic adenosine monophosphate (cAMP). Recent studies suggested that cAMP regulates several signaling pathways involved in the development and progression of renal disease, including mitogenesis, inflammation, and extracellular matrix synthesis. Cilostazol administration in streptozotocin-induced diabetic rats was reported to improve diabetic nephropathy as well as significantly decrease reactive oxygen species activity in the kidneys. In addition, cilostazol improved the serum cholesterol, triglyceride, and low density lipoprotein-cholesterol levels. Transforming growth factor-b and nuclear factor-kB are up-regulated in diabetic kidneys, but cilostazol treatment reduced the expression of these proteins. In conclusion, the ability of cilostazol to reduce oxidative stress and improve dyslipidemia may prevent the progression of diabetic nephropathy and diminish the risk of cardiovascular disease in diabetic patients.