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-β, 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.

Keywords: Diabetic kidney disease, Pathophysiology, Treatment