Deng Y L, Liu Y L, Tao Z W, Wang X
Department of Urology, the First Affiliated Hospital of Guangxi Medical University, Nanning 530021, China.
Zhonghua Wai Ke Za Zhi. 2018 Oct 1;56(10):733-736. doi: 10.3760/cma.j.issn.0529-5815.2018.10.004.
Calcium oxalate nephrolithiasis is the common disease of urinary surgery, its exact pathogenesis is still unclear.It is believed that the renal inflammatory injury induced by cell-crystal reaction plays an important role in the formation of intrarenal calcium oxalate crystals. Recent studies indicated that inflammation induced by cell-crystal reaction can cause renal cell damage, stimulate intracellular expression of NADPH oxidase, trigger the massive production of reactive oxygen species, activate nuclear factor-κB signaling pathway, release a large number of inflammatory factors, and cause inflammatory cascade effect of the kidney, thus promoting the accumulation, nucleation and growth of calcium salt crystals, eventually leading to the formation of intrarenal crystals and even stones. In this process, the regulatory factors and mechanisms involved include macrophages, NLRP3-high mobility group box-1 protein inflammation network, fetuin A, autophagy activation and other factors.
草酸钙肾结石是泌尿外科的常见疾病,其确切发病机制尚不清楚。据信,细胞-晶体反应诱导的肾炎症损伤在肾内草酸钙晶体形成中起重要作用。最近的研究表明,细胞-晶体反应诱导的炎症可导致肾细胞损伤,刺激细胞内NADPH氧化酶表达,引发活性氧大量产生,激活核因子-κB信号通路,释放大量炎症因子,引起肾脏炎症级联效应,从而促进钙盐晶体的积聚、成核和生长,最终导致肾内晶体甚至结石的形成。在此过程中,涉及的调节因子和机制包括巨噬细胞、NLRP3-高迁移率族蛋白1炎症网络、胎球蛋白A、自噬激活等因素。