Dysregulated coagulation system links to inflammation in diabetic kidney disease

Mengyun Xiao, D. Tang, Shaodong Luan, Bo Hu, Wenyu Gong, Wolfgang Pommer, Yong Dai, Lianghong Yin
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Abstract

Diabetic kidney disease (DKD) is a significant contributor to end-stage renal disease worldwide. Despite extensive research, the exact mechanisms responsible for its development remain incompletely understood. Notably, patients with diabetes and impaired kidney function exhibit a hypercoagulable state characterized by elevated levels of coagulation molecules in their plasma. Recent studies propose that coagulation molecules such as thrombin, fibrinogen, and platelets are interconnected with the complement system, giving rise to an inflammatory response that potentially accelerates the progression of DKD. Remarkably, investigations have shown that inhibiting the coagulation system may protect the kidneys in various animal models and clinical trials, suggesting that these systems could serve as promising therapeutic targets for DKD. This review aims to shed light on the underlying connections between coagulation and complement systems and their involvement in the advancement of DKD.
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凝血系统失调与糖尿病肾病的炎症有关
糖尿病肾病(DKD)是世界范围内终末期肾脏疾病的重要贡献者。尽管进行了广泛的研究,但其发展的确切机制仍然不完全清楚。值得注意的是,糖尿病和肾功能受损的患者表现出高凝状态,其特征是血浆中凝血分子水平升高。最近的研究表明,凝血酶、纤维蛋白原和血小板等凝血分子与补体系统相互关联,引起炎症反应,可能加速DKD的进展。值得注意的是,在各种动物模型和临床试验中,研究表明抑制凝血系统可以保护肾脏,这表明这些系统可以作为DKD的有希望的治疗靶点。这篇综述旨在阐明凝血和补体系统之间的潜在联系及其在DKD进展中的参与。
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