DIABETIC NEPHROPATHY: A NARRATIVE REVIEW FROM PATHOPHYSIOLOGY TO ITS TREATMENT

One of the most dangerous microvascular side effects of diabetes mellitus is diabetic nephropathy (DN), which is the primary cause of end-stage renal disease globally. Because type 2 diabetes, obesity, sedentary behavior, and metabolic syndrome are becoming more common, its occurrence is continuously rising, especially in developing countries. Persistent hyperglycemia, hemodynamic abnormalities, oxidative stress, hereditary vulnerability, and activation of inflammatory and profibrotic pathways are all part of the complex pathophysiology of diabetic kidney disease (DN), which leads to progressive renal impairment. Clinically, DN develops gradually and frequently shows no symptoms at first. Microalbuminuria is usually the first symptom, followed by persistent proteinuria, a drop in estimated glomerular filtration rate (eGFR), and finally renal failure. For prognosis and treatment, early diagnosis is crucial and depends on regular monitoring of the urine albumin-to-creatinine ratio and eGFR in addition to KDIGO staging. To distinguish non-diabetic renal diseases, renal biopsies are only performed in unusual circumstances. Strict blood pressure and glucose control, suppression of the renin-angiotensin-aldosterone system, and dietary and exercise changes are the mainstays of management. SGLT2 inhibitors, GLP-1 receptor agonists, and new anti-inflammatory and anti-fibrotic medications are examples of emerging treatments that have encouraging Reno protective benefits. Despite improvements, DN remains a significant global health and financial burden, underscoring the necessity of early screening, individualized care, and ongoing research.