Glomerular hyperfiltration predisposes nephron susceptible to damage irreversibly, thereby playing an important role in initiating the development of diabetic kidney disease. The pathogenesis of glomerular hyperfiltration in the past clinical trials has emphasized the importance of neurohormones such as the reninangiotensin-aldosterone system (RAAS). Unfortunately, diabetic kidney damage or glomerular hyperfiltration does not completely get attenuated by RAAS blockade. Therefore, many recent clinical trials have focused on role of renal tubular factors to the hyperfiltration state such as the sodium-glucose cotransporter. The tubular factors are acting to increase sodium reabsorption in the renal proximal tubule through sodium-glucose Cotransporter-2 as the leading cause of hyperfiltration by afferent arteriole dilation via the tubuloglomerular feedback. Clinical evidence has suggested that sodium-glucose cotransporter-2 inhibitors (SGLT2i) can not only reduce development but attenuate deterioration of albuminuria through various mechanisms. This review aims to discuss the role of SGLT2i in type 2 diabetes patients with chronic kidney disease in detail.