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糖尿病肾病(diabetic nephropathy,DN)已成为全球终末期肾病(end-stage renal diseas,ESRD)最常见的原因之一。在欧美发达国家20%~40%的糖尿病患者并发DN,最终成为透析治疗患者的首要原因[l]。DN的发生发展与遗传易感性、糖代谢紊乱、肾脏血流动力学异常、氧化应激、炎症反应及纤维增生等病理生理机制有关。现行干预DN的方法主要是强化血糖控制,应用肾素-血管紧张素-醛固酮系统(RAAS)拮抗剂和钙离子通道阻断剂降血压,但这些干预措施只是部分有效。如果要使DN的预期危害进一步降低,需要有新的肾脏保护干预措施[2]。因此,除遗传易感性外,针对上述病理生理环节新的靶向治疗手段不断涌现。?
Diabetic nephropathy (DN) has become one of the most common causes of end-stage renal disease (ESRD) in the world. In developed countries in Europe and the United States 20% to 40% of diabetic patients with DN, eventually became the primary cause of dialysis patients [1]. The occurrence and development of DN are related to the pathophysiological mechanisms such as genetic predisposition, disorders of glucose metabolism, abnormal renal hemodynamics, oxidative stress, inflammatory reaction and fibrogenesis. The current interventions for DN are mainly the intensification of glycemic control, the use of the renin-angiotensin-aldosterone system (RAAS) antagonist and calcium channel blockers to lower blood pressure, but these interventions are only partially effective. If we want to further reduce the expected harm of DN, new kidney protection interventions are needed [2]. Therefore, in addition to the genetic susceptibility, the new pathways for the pathophysiology of targeted therapies continue to emerge. ?