Diabetic nephropathy is a leading cause of
end-stage renal failure, which could account for disabilities and high mortality rates in patients with diabetes.
Diabetic nephropathy seems to occur as a result of an interaction between metabolic and hemodynamic factors, which activate common pathways that lead to renal damage. Recent large prospective clinical studies have shown that intensive
glucose control reduces microvascular complications effectively among patients with diabetes, and the renin-angiotensin system (RAS) is also an important target for both metabolic and hemodynamic derangements in
diabetic nephropathy. High
glucose, via various mechanisms such as increased production of oxidative stress and
advanced glycation end products (AGEs), activation of the RAS and
protein kinase C (PKC), and stimulation of the
polyol pathway, elicits vascular
inflammation and alters gene expression of
growth factors and
cytokines, thereby it might be involved in the development and progression of
diabetic nephropathy. Therefore, to develop novel therapeutic strategies that specifically target these metabolic and hemodynamic derangements is desired for patients with
diabetic nephropathy. In this review, we discuss the molecular mechanisms of
diabetic nephropathy and review the promising therapeutic targets for this devastating disorder.