Wang Jiayi, Zhong Jianyong, Yang Hai-Chun, Fogo Agnes B
1 Division of Nephrology, Second Xiangya Hospital, Central South University, Changsha, China.
2 Department of Pathology, Microbiology, and Immunology, Vanderbilt University Medical Center, Nashville, Tennessee, USA.
Toxicol Pathol. 2018 Dec;46(8):944-948. doi: 10.1177/0192623318796784. Epub 2018 Aug 29.
Tubular injury sensitizes glomeruli to injury. We review potential mechanisms of this tubuloglomerular cross talk. In the same nephron, tubular injury can cause stenosis of the glomerulotubular junction and finally result in atubular glomeruli. Tubular injury also affects glomerular filtration function through tubuloglomerular feedback. Progenitor cells, that is, parietal epithelial cells and renin positive cells, can be involved in repair of injured glomeruli and also may be modulated by tubular injury. Loss of nephrons induces additional workload and stress on remaining nephrons. Hypoxia and activation of the renin-angiotensin-aldosterone system induced by tubular injury also modulate tubuloglomerular cross talk. Therefore, effective therapies in chronic kidney disease may need to aim to interrupt this deleterious tubuloglomerular cross talk.
肾小管损伤会使肾小球对损伤更敏感。我们综述了这种肾小管 - 肾小球相互作用的潜在机制。在同一个肾单位中,肾小管损伤可导致肾小球 - 肾小管连接部狭窄,最终导致无肾小管的肾小球。肾小管损伤还通过肾小管 - 肾小球反馈影响肾小球滤过功能。祖细胞,即壁层上皮细胞和肾素阳性细胞,可参与受损肾小球的修复,也可能受到肾小管损伤的调节。肾单位的丧失会给剩余的肾单位带来额外的工作量和压力。肾小管损伤诱导的缺氧和肾素 - 血管紧张素 - 醛固酮系统的激活也会调节肾小管 - 肾小球相互作用。因此,慢性肾脏病的有效治疗可能需要旨在中断这种有害的肾小管 - 肾小球相互作用。