Paper Contents
Abstract
Diabetic nephropathy is also termed diabetic kidney disease is a major microvascular complication of diabetes mellitus and a leading cause of end-stage renal disease worldwide. DM is characterized by chronic hyperglycaemia due to insulin deficiency or resistance, significantly increases the risk of kidney damage through both metabolic and hemodynamic pathways. Diabetic nephropathy is characterized by mesangial enlargement, thickening of the glomerular basement membrane, a decrease in glomerular filtration rate, and persistent albuminuria and KimmelstielWilson nodules. Key modifiable risk factors include poor glycaemic control, hypertension, and dyslipidaemia, with genetic predisposition also contributing. Pathophysiology involves hyperglycaemia-induced oxidative stress, protein kinase C activation, renin-angiotensin-aldosterone system (RAAS) hyperactivity, and advanced glycation end products, resulting in inflammation, fibrosis, and progressive nephron loss. Diagnosis relies on albuminuria measurement and GFR estimation, with early detection crucial for intervention. Management focuses on stringent blood glucose control (HbA1c <7%), blood pressure reduction (preferably with ACE inhibitors or ARBs), lipid regulation (statins, fibrates), and lifestyle modifications including dietary salt restriction. Novel therapies such as SGLT2 inhibitors, GLP-1 receptor agonists, and PPAR agonists show Reno protective potential. In advanced cases, dialysis, kidney transplantation, or combined pancreaskidney transplantation may be indicated. Preventive strategies emphasize regular screening, multidisciplinary care, and patient education to delay disease progression and reduce cardiovascular risk. This review synthesizes current understanding of DNs epidemiology, pathophysiology, diagnosis, and treatment, highlighting the need for integrated therapeutic approaches to mitigate its global burden.
Copyright
Copyright © 2025 Mr. A. MOHAMMOD ARKAM. This is an open access article distributed under the Creative Commons Attribution License.
