[The role of cell-crystal reaction mediated inflammation in the formation of intrarenal calcium oxalate crystals]

Zhonghua Wai Ke Za Zhi. 2018 Oct 1;56(10):733-736. doi: 10.3760/cma.j.issn.0529-5815.2018.10.004.
[Article in Chinese]

Abstract

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病,其形成机制迄今不明。目前认为,细胞-晶体反应诱导的肾脏炎症损伤在肾内草酸钙晶体的形成过程中扮演着十分重要的角色。新近的研究结果显示,细胞-晶体反应介导的炎症可以导致肾脏细胞损伤,刺激细胞内的NADPH氧化酶表达,引发活性氧簇大量生成,激活核因子κB信号转导通路,释放大量的炎性因子,引发炎症级联反应,促进钙盐晶体的聚集、成核和生长过程,最终导致肾内晶体乃至结石的形成。巨噬细胞、NLRP3-高迁移率族蛋白炎症网络、胎球蛋白A、自噬激活等多种调控因子和作用机制参与这一过程。.

Keywords: Calcium oxalate; Inflammation; Kidney calculi.

MeSH terms

  • Autophagy
  • Calcium Oxalate* / metabolism
  • Humans
  • Inflammation*
  • Kidney / immunology
  • Kidney Calculi
  • Nephrolithiasis* / immunology

Substances

  • Calcium Oxalate