Review on pathophysiology and treatment of diabetic kidney disease

Diabetes is the leading cause of chronic kidney disease, which in the Thailand is the most common cause of end stage renal disease (ESRD) requiring dialysis. Patients with diabetic kidney disease (DKD) are at a higher risk of mortality, mostly from cardiovascular complications, than other patients with diabetes. The development of DKD is determined by environmental and genetic factors. This review focuses on the latest published data dealing with mechanisms and treatment of DKD. DKD has several distinct phases of development of the disease and hyperglycemia-induced metabolic and hemodynamic pathways are recognized to be mediators of kidney disease. Multiple biochemical pathways have been postulated that explain how hyperglycemia causes tissue damage: nonenzymatic glycosylation that generates advanced glycosylation end products, activation of protein kinase C, and acceleration of the polyol pathway. Oxidative stress also seems to be a theme common pathway. These derangements, along with hemodynamic changes, activate various cytokines and growth factors such as vascular endothelial growth factor, transforming growth factor-beta2 Interleukin 1 (IL 1), IL-6 and IL-18. Current renoprotective treatments for DKD include optimization of glycemic, blood pressure, lipid and weight control blockade of the renin-angiotensin system, salt and protein restriction. Multiple intensive interventions reduce cardiovascular events as well as nephropathy by about half when compared with a conventional multifactorial treatment.