Diabetic kidney disease (DKD) is a significant complication of diabetes mellitus with limited treatment options. The progression of DKD is marked by substantial lipid disturbances, including changes in triglycerides, cholesterol, sphingolipids, phospholipids, lipid droplets, and bile acids. Altered lipid metabolism plays a crucial role in DKD pathogenesis, potentially linked to cellular ferroptosis, lipophagy, lipid metabolism reprogramming, and immune modulation of gut microbiota, which affects the liver-kidney axis. Understanding these mechanisms opens new therapeutic pathways for DKD management. DKD is characterized by glomerular pathology, including diffuse and nodular glomerular basement membrane thickening, tubular atrophy, interstitial inflammation, fibrosis, glomerular endothelial injury, podocyte loss, and glomerular vascular hyalinopathy. DKD pathogenesis is complex, involving glucose and lipid metabolism disorders and stress. Current treatments, such as glycemic control and urinary albumin reduction, do not fundamentally alter the course of DKD. New guidelines recommend ACEIs/ARBs and novel hypoglycemic agents, but these have not been found to slow DKD progression. Lipid metabolism disorders in DKD involve abnormalities in lipid metabolism, such as triglycerides, cholesterol, and lipid droplets. Recent studies have explored the mechanisms of lipid metabolism disorder in DKD, including ferroptosis, which is a programmed death resulting from lipid peroxidation and is closely related to lipid metabolism disorders. Another mode of programmed death is associated with defects in the autophagy-lysosomal system and abnormal lipid accumulation in podocytes. Lipid metabolism reprogramming results in dysfunctional lipid uptake and oxidation, especially of fatty acids, which are exacerbated in DKD. Imbalance of gut microbiota and increased intestinal barrier permeability, a pathological manifestation of DKD, and its involvement in immune imbalance, especially involving the liver-kidney axis, affect lipid metabolism, such as bile acid metabolism, and the immune imbalance aggravates renal injury. Abnormalities in the metabolism of triglycerides, cholesterol, sphingolipids, phospholipids, lipid droplets, and bile acids are key factors in DKD progression. Both the quality and quantity of lipids are associated with this process and produce reactive oxygen species (ROS), which exacerbate oxidative stress, inflammation, and cell death. Abnormal triglyceride metabolism in DKD is mainly characterized by abnormal uptake and oxidation of fatty acids. Fatty acid transport proteins, cluster of differentiation 36, and fatty acid-binding protein are correlated with FA uptake in DKD. Fatty acid oxidation is the primary pathway that reduces the renal lipid content. The expression of FAO genes was significantly reduced in DKD. Abnormal cholesterol metabolism in DKD is closely associated with DKD. Studies have demonstrated that increased expression of sterol regulatory element-binding proteins and isoDiabetic kidney disease (DKD) is a significant complication of diabetes mellitus with limited treatment options. The progression of DKD is marked by substantial lipid disturbances, including changes in triglycerides, cholesterol, sphingolipids, phospholipids, lipid droplets, and bile acids. Altered lipid metabolism plays a crucial role in DKD pathogenesis, potentially linked to cellular ferroptosis, lipophagy, lipid metabolism reprogramming, and immune modulation of gut microbiota, which affects the liver-kidney axis. Understanding these mechanisms opens new therapeutic pathways for DKD management. DKD is characterized by glomerular pathology, including diffuse and nodular glomerular basement membrane thickening, tubular atrophy, interstitial inflammation, fibrosis, glomerular endothelial injury, podocyte loss, and glomerular vascular hyalinopathy. DKD pathogenesis is complex, involving glucose and lipid metabolism disorders and stress. Current treatments, such as glycemic control and urinary albumin reduction, do not fundamentally alter the course of DKD. New guidelines recommend ACEIs/ARBs and novel hypoglycemic agents, but these have not been found to slow DKD progression. Lipid metabolism disorders in DKD involve abnormalities in lipid metabolism, such as triglycerides, cholesterol, and lipid droplets. Recent studies have explored the mechanisms of lipid metabolism disorder in DKD, including ferroptosis, which is a programmed death resulting from lipid peroxidation and is closely related to lipid metabolism disorders. Another mode of programmed death is associated with defects in the autophagy-lysosomal system and abnormal lipid accumulation in podocytes. Lipid metabolism reprogramming results in dysfunctional lipid uptake and oxidation, especially of fatty acids, which are exacerbated in DKD. Imbalance of gut microbiota and increased intestinal barrier permeability, a pathological manifestation of DKD, and its involvement in immune imbalance, especially involving the liver-kidney axis, affect lipid metabolism, such as bile acid metabolism, and the immune imbalance aggravates renal injury. Abnormalities in the metabolism of triglycerides, cholesterol, sphingolipids, phospholipids, lipid droplets, and bile acids are key factors in DKD progression. Both the quality and quantity of lipids are associated with this process and produce reactive oxygen species (ROS), which exacerbate oxidative stress, inflammation, and cell death. Abnormal triglyceride metabolism in DKD is mainly characterized by abnormal uptake and oxidation of fatty acids. Fatty acid transport proteins, cluster of differentiation 36, and fatty acid-binding protein are correlated with FA uptake in DKD. Fatty acid oxidation is the primary pathway that reduces the renal lipid content. The expression of FAO genes was significantly reduced in DKD. Abnormal cholesterol metabolism in DKD is closely associated with DKD. Studies have demonstrated that increased expression of sterol regulatory element-binding proteins and iso