Renal senescence is accompanied by a gradual decrease in its function. Although it rarely causes clinical problems per se, superimposition of various diseases, such as diabetes, may accelerate this functional decline. Recent research has revealed some of the complex mechanisms of how diabetes promotes the aging process in the kidney, including the pathogenic roles of hemodynamic changes, tubulointerstitial hypoxia, oxidative stress, advanced glycation end-products, and impaired autophagy. Diabetes also modulates aging-related signaling pathways, such as sirtuins and mammalian target of rapamycin. Current therapeutic strategy for diabetic kidney disease consists of glycemic control and antihypertensive treatment with renin- angiotensin system inhibitors. However, they fail to fully prevent the progression of diabetic kidney disease, raising an urgent need for novel therapeutic methods. Some pharmacological agents are being developed based on the knowledge of hemodynamic and molecular basis of diabetes- and aging-related kidney function decline.