Sodium-Glucose Transporter Type 2 (SGLT2) Inhibitor for Diabetic Kidney

In diabetes, both activation of renin-angiotensin system and glomerular hyperfiltration are seen even before the development of diabetic nephropathy. Glomerular hyperfiltration depends on glomerular hypertension sue to pathophysiological afferent arteriolar dilation. Tubular hypothesis has been proposed more than a decade ago to explain the above in type1 diabetes. Recently, clinical evidences have been accumulated to support tubular hypothesis functioning in type2 diabetes. In addition to intrinsic renal hemodynamic physiology, the key molecule for tubular hypothesis is sodium glucose co-transporter in proximal tubules. Thus, application of sodium glucose co-transporter for diabetes may provide a break-through for the management of diabetes in preventing the development of nephropathy. Recently, SGLT2 inhibitors,a new anti-diabetic drug, have become available for clinical use. This drug is superior to classical anti-diabetic medications such as sulfonyl urea and metoformin, facilitating weight loss and decreasing systolic blood pressure [1]. In addition to their excellent anti-diabetic actions, they could prevent the development of diabetic nephropathy. Potential renal hemodynamic mechanisms for renal protection by this medication are reviewed.