Diabetic kidney disease (DKD) is a glomerular disease caused by metabolic disorders that impair renal cell function. Mitochondria, crucial for energy production through oxidative phosphorylation, play a key role in metabolic reprogramming, a process that allows cells to adapt to energy demands. In DKD, mitochondrial metabolic reprogramming significantly influences disease progression, leading to oxidative stress, inflammation, apoptosis, and autophagy, which contribute to renal fibrosis and insufficiency. This review highlights the role of mitochondrial metabolic reprogramming in DKD pathogenesis, emphasizing the regulation of metabolic regulators and downstream signaling pathways. Therapeutic interventions targeting renal metabolic reprogramming may help delay DKD progression. Current treatments for DKD, such as intensive glucose lowering and blood pressure control, can slow disease progression but have limitations. Newer hypoglycemic agents, including SGLT2 inhibitors and GLP-1 agonists, can delay DKD progression by regulating metabolic reprogramming. However, the safety and efficacy of these drugs in altering DKD progression require further investigation. The review discusses the impact of mitochondrial metabolic reprogramming in different types of renal cells, including renal tubular epithelial cells, podocytes, mesangial cells, and glomerular endothelial cells. It also summarizes various treatments for DKD, including traditional and emerging therapies. Emerging therapies can delay or prevent end-stage renal disease (ESRD) by intervening in metabolic reprogramming. Future strategies may involve modulating mitochondrial reprogramming and restoring substance metabolism. The review also explores the metabolic processes in the kidney, including glucose, lipid, and protein metabolism, and their roles in DKD. Metabolic reprogramming in DKD is associated with changes in energy metabolism, lipid metabolism, and amino acid metabolism, leading to cellular damage and fibrosis. The review highlights the importance of understanding the mechanisms of metabolic reprogramming in DKD and developing new therapeutic strategies.Diabetic kidney disease (DKD) is a glomerular disease caused by metabolic disorders that impair renal cell function. Mitochondria, crucial for energy production through oxidative phosphorylation, play a key role in metabolic reprogramming, a process that allows cells to adapt to energy demands. In DKD, mitochondrial metabolic reprogramming significantly influences disease progression, leading to oxidative stress, inflammation, apoptosis, and autophagy, which contribute to renal fibrosis and insufficiency. This review highlights the role of mitochondrial metabolic reprogramming in DKD pathogenesis, emphasizing the regulation of metabolic regulators and downstream signaling pathways. Therapeutic interventions targeting renal metabolic reprogramming may help delay DKD progression. Current treatments for DKD, such as intensive glucose lowering and blood pressure control, can slow disease progression but have limitations. Newer hypoglycemic agents, including SGLT2 inhibitors and GLP-1 agonists, can delay DKD progression by regulating metabolic reprogramming. However, the safety and efficacy of these drugs in altering DKD progression require further investigation. The review discusses the impact of mitochondrial metabolic reprogramming in different types of renal cells, including renal tubular epithelial cells, podocytes, mesangial cells, and glomerular endothelial cells. It also summarizes various treatments for DKD, including traditional and emerging therapies. Emerging therapies can delay or prevent end-stage renal disease (ESRD) by intervening in metabolic reprogramming. Future strategies may involve modulating mitochondrial reprogramming and restoring substance metabolism. The review also explores the metabolic processes in the kidney, including glucose, lipid, and protein metabolism, and their roles in DKD. Metabolic reprogramming in DKD is associated with changes in energy metabolism, lipid metabolism, and amino acid metabolism, leading to cellular damage and fibrosis. The review highlights the importance of understanding the mechanisms of metabolic reprogramming in DKD and developing new therapeutic strategies.