Division of Nephrology, Department of Medicine, Tri-Service General Hospital, National Defense Medical Center, Taipei, Taiwan.
Adv Clin Chem. 2012;56:55-74. doi: 10.1016/b978-0-12-394317-0.00014-5.
Diabetic nephropathy (DN), the most common cause of end-stage renal disease (ESRD), is increasingly considered an inflammatory process characterized by leukocyte infiltration at every stage of renal involvement. Cytokines act as pleiotropic polypeptides that regulate inflammatory and immune responses, providing important signals in the pathologic and physiologic processes. Inflammation and activation of the immune system are closely involved in the pathogenesis of diabetes and its microvascular complications. Proinflammatory, Th1, Th2, and Th17 cytokines, as well as TGF-beta, all take part in the development and progression of DN. Gene polymorphism of cytokines and their receptors may have functional variations and can be applied to predict the susceptibility and progression to DN. Improved knowledge on recognizing cytokines as significant pathogenic mediators in DN leaves opens the possibility of new potential therapeutic agents for future clinical treatments.
糖尿病肾病（DN）是终末期肾病（ESRD）最常见的病因，越来越多的研究认为它是一种炎症过程，在肾脏受累的各个阶段都有白细胞浸润。细胞因子作为多效性多肽，调节炎症和免疫反应，在病理和生理过程中提供重要信号。炎症和免疫系统的激活与糖尿病及其微血管并发症的发病机制密切相关。促炎细胞因子、Th1、Th2 和 Th17 细胞因子以及 TGF-β均参与 DN 的发生和发展。细胞因子及其受体的基因多态性可能具有功能差异，并可用于预测 DN 的易感性和进展。对细胞因子作为 DN 重要致病介质的认识的提高，为未来临床治疗提供了新的潜在治疗药物的可能性。
