Diabetic nephropathy (DN) is a leading cause of mortality and morbidity, decreases quality of life and shortened life expectancy. The renin angiotensin system is considered to be involved in most of the pathological processes that result in diabetic nephropathy. Various subsystems of RAAS contribute to the disease pathology. One of these involves angiotensin II (Ang II) which shows increased activity during diabetic nephropathy. Evidence indicates interaction between advanced glycation end products (AGEs), activated protein kinase C (PKC) and angiotensin II provoke the progression of DN. Inhibitors of angiotensin-converting enzyme (ACEIs), renin angiotensin aldosterone system (RAAS), AGEs, and PKC have been tested for slowing down the progression of DN. This review focuses on the latest published data dealing with the pathophysiology, stages of DN, pathogenesis, prevention and treatment of DN.

Background: Kidney disease is a universal public health problem, and epidemiological studies demonstrated that the incidences of chronic kidney disease are increasing day by day. However, the efficiency of currently available drugs on the progression of nephropathy is limited. Therefore, the current research was designed to evaluate the therapeutic efficacy of captopril and BQ123 against hyperlipidemia-induced nephropathy in rats. Objective: Implication of Endothelin-1 in Experimentally Induced Hyperlipedemic Nephropathy in Rats Methods: Animals were divided into various groups, and the administration of a high-fat diet for six weeks induced hyperlipidemia. After confirmation of hyperlipidemia, treatment was started for the next 14 days. At the end of the experimental period, the animals were sacrificed, and various biochemical parameters and histopathological studies were performed. Results: Treatment of both the agents in combination effectively decreased BUN levels, serum creatinine, serum nitrite, and proinflammatory markers and ameliorated the pathological injuries of kidneys. Conclusion: Furthermore, both treatments also inhibited oxidative stress and restored the hyperlipidemia-induced reduction in the level of antioxidant enzymes.