Abstract
BACKGROUND: Diabetes is the leading cause of end-stage renal disease (ESRD) and accounts for 40-50% of patients requiring renal replacement therapy. The main pathophysiology of diabetic nephropathy comprises glucose-dependent pathways, hemodynamic pathways, and genetic factors. SUMMARY: Glucose-dependent pathways, known as advanced glycation, polyols, and protein kinase C activation have been implicated in the pathogenesis of diabetic nephropathy. Current studies have indicated that intensified glycemic control retards the rate of development of albuminuria and impairs renal function in both patients with type 1 and 2 diabetes. However, therapeutic options have substantially increased over the last decade, but have not yet been translated to remarkably reduce the incidence of ESRD from diabetic nephropathy. Sodium-glucose cotransporter 2 (SGLT2) inhibitors are a novel class of glucose-lowering agents with potential renoprotective effects. KEY MESSAGE: SGLT2 inhibitors represent a promising therapeutic approach to prevent and improve nephropathy among patients with type 2 diabetes. The current data strongly support that SGLT2 inhibitors have renoprotective properties not only by improving glycemic control but also through hemodynamic and nonhemodynamic renal effects. This review focuses on the latest published data dealing with hypoglycemic agents and SGLT2 inhibitors regarding the progression of kidney disease.