Diabetische Nephropathie: Neues zur Pathogenese [Diabetic nephropathy: update on pathogenesis]

Diabetes mellitus is the most common cause of renal failure in industrialized countries. It is largely unknown why only 20 -40% of patients with diabetes develop diabetic nephropathy. Experimental animal models with histological features of human diabetic nephropathy could help to elucidate new genetic and pathophysiological mechanisms of diabetic nephropathy. The benefit of intensive blood glucose control has been well documented for renal endpoints in Type 1 diabetes (DCCT EDIC). In contrast, major clinical diabetes intervention studies (ACCORD, ADVANCE, VA DIABETES) were not able to demonstrate convincing benefits of tight blood sugar control in Type 2 diabetes. Nevertheless, these studies revealed novel outcome-derived hypotheses. Genome-wide association studies (GWAS) have been completed to identify genetic loci on chromosomes for a genetic predisposition of diabetic nephropathy in humans. This review reports on recent results on the establishment of suitable mouse models that mimic human diabetic nephropathy, aspects of renal endpoints in the therapeutic objectives of diabetics, and new insights into the genetic predisposition (susceptibility) of diabetic nephropathy in humans