The Role of ACE Inhibitors in Slowing Diabetic Nephropathy Progression: A Comprehensive Review

Diabetic nephropathy (DN), a significant microvascular complication of diabetes mellitus, is a major cause of end-stage renal disease globally. Chronic hyperglycemia, renin-angiotensin-aldosterone system (RAAS) activation, oxidative stress, and inflammation are among the metabolic and hemodynamic variables that interact intricately in the pathophysiology of diabetic nephropathy (DN), which results in progressive glomerular damage and fibrosis. Because of their capacity to alter RAAS activity, lower intraglomerular pressure, and lessen structural kidney damage, angiotensin-converting enzyme (ACE) inhibitors have become a mainstay in the treatment of diabetic kidney disease (DN). ACE inhibitors have renoprotective benefits in addition to lowering blood pressure because they reduce proteinuria, mitigate mesangial expansion, and restrict the buildup of extracellular matrix. This review summaries data from observational studies, clinical trials, and meta-analyses assessing the safety and effectiveness of ACE inhibitors in delaying the progression of DN. Large randomized trials have repeatedly shown that patients on ACE inhibitors, especially in the early stages of DN, have lower albuminuria and a delayed start of end-stage renal disease. Alongside suggested monitoring, safety factors such as hyperkalaemia, coughing, and acute renal injury are covered. With specific blood pressure objectives and initiation criteria, ACE inhibitors are strongly recommended as first-line therapy in DN by current clinical guidelines. This review demonstrates the critical role that ACE inhibitors play in the treatment of DN by combining pathophysiological insights, mechanistic data, and clinical evidence. Even with their proven advantages, more research is necessary to improve therapy, investigate combination regimens, and tailor treatment plans according to phenotypic and genetic characteristics.