Endocrine Abstracts

At present, diabetic kidney disease affects about 15-25 % of all type 1 diabetic patients and 20-40 % of all patients with type 2 diabetes. The mechanisms underlying the development of diabetic kidney disease are extremely complex and not yet fully understood. Among many potential pathogenic mechanisms responsible for the progression in diabetic nephropathy, metabolic factors beyond blood glucose, e.g. advanced glycation end-products (AGEs), and growth factors/cytokines have been suggested to be involved. Examples of the latter are transforming growth factor b (TGF-b), connective tissue growth factor (CTGF), growth hormone (GH), insulin-like growth factors (IGFs) and vascular endothelial growth factor (VEGF). Recent findings that these systems initiate the early diabetic renal changes have provided insight into processes that might be relevant for future development of drugs useful in the treatment of the disease. Accordingly, these studies have enhanced the understanding of the cellular mechanisms responsible for the initiation and progression of diabetic kidney disease and have allowed development of specific antagonists of pathophysiologically elevated levels of AGEs and growth factors. Studies have shown that treating experimental diabetic animal models with such antagonists is followed by renoprotection and accordingly new therapeutic strategies have been suggested.