Oxidative stress in diabetic kidney disease

Diabetic Kidney Disease (DKD) represents a worldwide public health problem, due to its ever growing incidence and high costs connected to the imposed therapies regarding substitution of kidney functions. DKD includes all the anatomical, clinical and functional alterations that occur at kidney level in a patient with Diabetes Mellitus (DM), as a result of numerous metabolic and haemodynamic factors at the level of kidney microcirculation, based on a polygenous genetical polymorphism that generates an individual susceptibility for this complication. DKD is found in 20-40% of DM patients and it represents the main cause of chronic kidney disease. In DKD pathogeny, an important part is played by the oxidative stress determined by hyperglycemia. Among the mechanisms by which hyperglycemia may affect the kidney we may enumerate polyol pathway activation, C protein-kinase activation (PKC), non-enzymatic protein glycosylation. Out of the highly reactive molecules involved in the oxidative stress of DKD, an important role is attributed to *O2-, *NO and ONOO-. The role of oxidative stress played in DKD pathogeny is also supported by the promising results of some antioxidant therapies in DKD: AGE inhibitors (pyridorin, 2,3 diamino-phenazine, bromo-phenylacetic thiazolium, aminoguanidine/pimagedine), diacylglycerol pathway inhibitors (vitamin E, thiamine, benfotiamine, aminoguanidine), PKC inhibitors (ruboxistaurin), transketolase activators (thiamine and benfotiamine).