ABSTRACT:
Diabetic Nephropathy (DN), or diabetic kidney disease, remains the leading cause of end-stage renal disease (ESRD) globally, affecting approximately 30% to 40% of patients with diabetes mellitus. This review explores the multifaceted renal risk factors—including chronic hyperglycemia, systemic hypertension, and genetic predisposition—that drive the progression from microalbuminuria to overt nephropathy. The pathogenesis involves complex biochemical pathways, notably the activation of the renin-angiotensin-aldosterone system (RAAS), oxidative stress, and the accumulation of advanced glycation end-products (AGEs). These factors contribute to glomerular hyperfiltration, podocyte injury, and progressive tubulointerstitial fibrosis. Management strategies have evolved significantly beyond traditional glycemic and blood pressure control. While ACE inhibitors and ARBs remain the foundational therapy for renal protection, the emergence of SGLT2 inhibitors and GLP-1 receptor agonists has redefined the treatment landscape by demonstrating significant reductions in albuminuria and the rate of eGFR decline. Furthermore, the introduction of non-steroidal mineralocorticoid receptor antagonists (MRAs) offers a novel pathway to mitigate inflammation and fibrosis. This abstract emphasizes an integrated, multidisciplinary approach to management, focusing on early screening, intensive risk factor modification, and the implementation of nephroprotective pharmacotherapy to improve long-term clinical outcomes.