Providence Health Care, Spokane, WA; Kidney Research Institute and Division of Nephrology, Seattle, WA; Institute of Translational Health Sciences, Seattle, WA; and the University of Washington School of Medicine, Seattle, WA.
Providence Health Care, Spokane, WA; Kidney Research Institute and Division of Nephrology, Seattle, WA; Institute of Translational Health Sciences, Seattle, WA; and the University of Washington School of Medicine, Seattle, WA.
Adv Chronic Kidney Dis. 2018 Mar;25(2):181-191. doi: 10.1053/j.ackd.2017.12.002.
Diabetic kidney disease (DKD) is the leading cause of CKD and end-stage kidney disease (ESKD) worldwide. Approximately 30-40% of people with diabetes develop this microvascular complication, placing them at high risk of losing kidney function as well as of cardiovascular events, infections, and death. Current therapies are ineffective for arresting kidney disease progression and mitigating risks of comorbidities and death among patients with DKD. As the global count of people with diabetes will soon exceed 400 million, the need for effective and safe treatment options for complications such as DKD becomes ever more urgent. Recently, the understanding of DKD pathogenesis has evolved to recognize inflammation as a major underlying mechanism of kidney damage. In turn, inflammatory mediators have emerged as potential biomarkers and therapeutic targets for DKD. Phase 2 clinical trials testing inhibitors of monocyte-chemotactic protein-1 chemokine C-C motif-ligand 2 and the Janus kinase/signal transducer and activator of transcription pathway, in particular, have produced promising results.
糖尿病肾病(DKD)是全球范围内导致慢性肾脏病(CKD)和终末期肾病(ESKD)的主要原因。大约 30-40%的糖尿病患者会出现这种微血管并发症,使他们面临肾功能丧失以及心血管事件、感染和死亡的高风险。目前的治疗方法对于阻止肾脏疾病进展以及减轻 DKD 患者的合并症和死亡风险无效。随着全球糖尿病患者人数即将超过 4 亿,对于 DKD 等并发症的有效和安全治疗选择的需求变得更加迫切。最近,对 DKD 发病机制的认识已经发展到将炎症视为肾脏损伤的主要潜在机制。反过来,炎症介质已成为 DKD 的潜在生物标志物和治疗靶点。特别是,测试单核细胞趋化蛋白-1 趋化因子 C-C 基序配体 2 和 Janus 激酶/信号转导和转录激活因子途径抑制剂的 2 期临床试验取得了有希望的结果。