Kidney cells have unique characteristics in their energy metabolism. Particularly, in the proximal tubular cells (PTECs), they physiologically maintain their ATP production via fatty acid oxidation (FAO) regardless of during fasting or feeding. Growing experimental evidences have shown that FAO-dependent ATP production in PTECs declines as the renal disease progresses, and the recovery of FAO is expected to be a novel therapeutic target for kidney diseases including diabetic kidney disease (DKD). Furthermore, in the damaged PTECs, glycolysis, which is originally thought to be absent in healthy PTECs, is abnormally activated, and this abberant glycolysis is likely to be also involved in the progression of DKD. In addition to fatty acids and glucose, ketone bodies are an additional ATP source for mammalian cells. Since ketone bodies are a necessary source of ATP, especially during long-term fasting, they are unnecessary for us living in the age of plenty, and have long been recognized as the bad guys because of ketoacidosis, a life-threatening event in diabetes. However, recent several findings obtained from anti-aging studies show the pivotal roles of ketone bodies for healthy longevity. We have also reported that ketone bodies have a reno-protective role against DKD via inhibition of renal mTORC1 signal, and that the improvement of ketone body metabolism is involved in the reno-protective mechanism of SGLT2 inhibitors, which have recently shown potent organ-protective effects in clinical practice. In an age of plenty, the importance of ketone bodies as an energy source during fasting is becoming less and less important, but the role of ketone bodies as not just a nutrient but also as an organ protector may shed new light in the world of diabetes care again in the future. In this lecture, I discuss the importance of renal ketone body metabolism as a promising therapeutic target for DKD.