Diabetic nephropathy is the largest single cause of end-stage renal disease (ESRD). It starts from microalbuminuria, an increased leakage of proteins into urine, and ends with renal failure, the building up of toxic waste in blood requiring dialysis or kidney transplantation. This process takes nearly 10 to 20 years to develop and occurs in about 20% of patients with diabetes. Hyperglycemia and the relevant metabolic disorders in diabetes can induce oxidative stress and inflammatory response in the body and the kidney in particular, eventually resulting in kidney fibrosis and the loss of function. Many molecules and pathways have been linked to contributing to renal damage. However, due to the complexity of diabetic nephropathy, there is no complete understanding of this devastating disease. Identifying novel biomarkers for early diagnosis and novel target(s) for treatment to prevent or slow the progression of renal damage in diabetics are a big challenge.

In this special issue of the Journal of Diabetes Research, we are inviting authors to submit original research papers as well as review articles to discuss the current understanding of cellular and molecular pathology, function, and signal pathways in diabetic nephropathy. We are also interested in manuscripts that report the advances in diagnosis or treatment of diabetic nephropathy.

Potential topics include, but are not limited to:

• Proteinuria in diabetic nephropathy: molecular and pathological basis
• In vivo and in vitro studies on podocyte, vascular endothelium, and tubular cell damage
• Oxidative stress and inflammation in diabetic kidney
• Fibrosis, what is the major driving factor?
• New pathway in diabetic nephropathy
• Novel approach to prevent or treat diabetic nephropathy