Pathogenesis of diabetic kidney disease

S. Tang, Anthony Chan, W. Yiu, K. Lai
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Abstract

Abstract Diabetic kidney disease (DKD) is characterized by an accumulation of extracellular matrix proteins such as collagen and fibronectin in the kidney, resulting in tubulointerstitial fibrosis, glomerular mesangial hypertrophy and expansion, thickening of the glomerular basement membrane, podocyte foot process effacement, and inflammation due to the infiltration of monocytes and macrophages. All of these factors contribute to kidney function loss and can ultimately lead to progressive chronic kidney disease and kidney failure. In the review, we summarize the current state of knowledge in the pathogenesis of diabetic kidney disease to include the impact of genetic and environmental factors, hemodynamic changes, glycemic control, inflammation, proteinuria and novel mechanisms such as non-coding RNAs and lipotoxicity.
糖尿病肾病的发病机制
糖尿病肾病(DKD)的特点是肾脏中胶原、纤连蛋白等细胞外基质蛋白的积累,导致肾小管间质纤维化、肾小球系膜肥大和扩张、肾小球基底膜增厚、足细胞足突消失以及单核细胞和巨噬细胞浸润引起的炎症。所有这些因素都会导致肾功能丧失,并最终导致进行性慢性肾病和肾衰竭。本文综述了糖尿病肾病发病机制的研究现状,包括遗传和环境因素的影响、血流动力学改变、血糖控制、炎症、蛋白尿以及非编码rna和脂肪毒性等新机制。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
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