Diabetic nephropathy is a common and serious complication of diabetes mellitus (DM), characterized by progressive kidney damage that can lead to end-stage renal disease (ESRD). It primarily affects individuals with both type 1 and type 2 diabetes, and its pathogenesis involves complex interplay of metabolic, hemodynamic, and inflammatory factors. Key mechanisms include hyperglycemia-induced oxidative stress, activation of the renin-angiotensin-aldosterone system (RAAS), and inflammatory pathways. Current therapeutic approaches aim to delay or prevent the progression of diabetic nephropathy. Tight glycemic control through lifestyle modifications and pharmacotherapy remains fundamental, as it helps reduce the incidence and progression of kidney disease. Additionally, renin-angiotensin system blockade with angiotensin-converting enzyme inhibitors (ACEIs) or angiotensin II receptor blockers (ARBs) is crucial in managing diabetic nephropathy due to their renoprotective effects, including reducing proteinuria and preserving kidney function. Beyond glucose and blood pressure control, newer therapeutic strategies involve the use of sodium-glucose co-transporter 2 (SGLT2) inhibitors, which have shown promising results in reducing renal events and slowing the decline in kidney function in patients with diabetic nephropathy. These agents exert their effects by inhibiting glucose reabsorption in the proximal tubule of the kidney, leading to glycosuria and natriuresis, and thereby reducing intraglomerular pressure and albuminuria. Furthermore, comprehensive management includes lifestyle modifications (such as dietary sodium restriction and smoking cessation), treatment of dyslipidemia, and regular monitoring of kidney function through urine albumin-to-creatinine ratio and estimated glomerular filtration rate (eGFR). Multidisciplinary care involving nephrologists, endocrinologists, and primary care providers is essential to optimize therapeutic strategies and improve outcomes in patients with diabetic nephropathy.