The role of insuline resistance in kidney injury

Abstract

Diabetes is complicated by diabetic nephropathy in ~50% of cases. Its occurrence is attributed to long-term influence of hyperglycemia on the kidneys. Nevertheless, studies of the recent 10 years have shown that pathogenesis of diabetic nephropathy also involves other disorders accompanying insulin resistance of peripheral tissues, as well as insulin resistance of kidney cells themselves. Insulin at physiological blood concentrations is vital for the intact structure of cytoskeleton, and thus conformation and function of the podocyte. Among the elements of the insulin resistance syndrome, hyperleptinemia augments glomerular fibrosis, whereas hypertriglyceridemia, plausibly along with hyperglycemia and hyperinsulinemia, deteriorates sensitivity of podocytes to insulin. The latter evokes functional and histological abnormalities typical for diabetic nephropathy. Another potential contributor to kidney damage in the course of diabetes is inadequate action of insulin on proximal tubule cells, which results in disturbed albumin endocytosis in experimental settings. The research performed so far, as well as that awaited, shall augment chances for kidney protection in diabetic patients.