In affluent nations like the United States, diabetic kidney disease (DKD) is the main contributor to end-stage kidney disease (ESKD). Both diabetes mellitus type 1 (T1DM) and diabetes mellitus type 2 are affected by this microvascular condition (T2DM). Albuminuria that doesn't go away and a steady drop in glomerular filtration rate are the symptoms of the condition. There is strong evidence that early intervention can halt or stop the disorder's course.Urine albuminuria and estimated GFR are reliable diagnostic and monitoring assays (eGFR). Stopping the advancement of DKD depends on maintaining optimal blood sugar levels and adequate blood pressure management. Reactive oxygen species are produced as a result of hyperglycemia, and processes such protein kinase C, polyol, hexosamine, and advanced glycation end products are activated (AGE). The presence of a substantial amount of cytokines and chemokines, including as IL-6, MCP-1, TGF-beta, and VEGF (vascular endothelial growth factor), that cause inflammation fibrosis and enhanced vascular permeability is a key characteristic. Albuminuria arises as a result of the ensuing podocytopathy. Proteinuria is the outcome of the resultant intraglomerular and systemic hypertension. Epithelial-mesenchymal cell transition brought on by proteinuria results in fibroblasts and persistent tubular damage. Diabetes nephropathy treatment focuses on lowering cardiovascular risk, managing blood sugar levels, regulating blood pressure, and inhibiting the renin-angiotensin system (RAS). For the purpose of lowering cardiovascular risk, risk-factor modification is essential. This includes quitting smoking and using the best lipid management techniques. High morbidity and death are associated with diabetic nephropathy. An independent risk factor for cardiovascular death is microalbuminuria. End-stage renal disease is the primary cause of death among patients. Additionally, diabetic nephropathy and diabetic retinopathy are linked.