Uric acid as a biomarker and a therapeutic target in diabetes

Diabetic nephropathy is a long-standing microvascular complication of diabetes mellitus and is the leading cause of end stage renal disease in developed countries. Current therapeutic strategies used to prevent or delay diabetic nephropathy exert limited clinical protective effects and can have serious adverse effects. Thus, identification of new pharmacologic agents that protect against the initiation and progression of complications of diabetes is of the utmost importance. Uric acid (UA) recently emerged as an inflammatory factor that increases oxidative stress and promotes activation of the renin angiotensin aldosterone system. As a consequence, higher UA levels are associated with various stages of the onset and progression of diabetic nephropathy, including metabolic, cardiovascular and kidney function abnormalities. If UA-lowering drugs, such as the xanthine oxidase inhibitors, block the mechanisms responsible for micro- and macrovascular injury in diabetes, these agents could represent a critical step toward preventing the progression of diabetes. This review focuses on the evidence that supports serum UA levels as a biomarker of renal and cardiovascular risk and as a potential additional therapeutic target in diabetes.