Cilostazol exerts antiplatelet, antithrombotic and vasodilating effects by inhibiting phosphodiesterase type 3 in platelets and vascular smooth muscle cells. Furthermore, cilostazol treatment has been shown to reduce serum triglyceride concentrations and increase HDL-cholesterol levels. In Japanese patients with type 2 diabetes, cilostazol therapy was associated with regression of carotid intimal media thickness and could prevent the onset of silent brain infarction. On the other hand, abnormal metabolism of prostaglandins in renal glomeruli has been postulated to modulate renal haemodynamics. Elevated levels of platelet-derived microparticles and soluble adhesion molecules may further contribute to the development of diabetic nephropathy. Cilostazol treatment had been shown to reduce serum levels of PMP, activated platelet subsets, soluble adhesion molecules and urinary excretion of thromboxane B2 in patients with type 2 diabetes. These changes were accompanied by a reduction in urinary albumin excretion and an increase in creatinine clearance.