Yang Li, Humphreys Benjamin D, Bonventre Joseph V
Contrib Nephrol. 2011;174:149-155. doi: 10.1159/000329385. Epub 2011 Sep 9.
After damage the kidney has the ability to repair itself. With mild injury this repair can result in the return to a structural and functional state that is indistinguishable from normal. However, when the repair is more severe or is superimposed on baseline kidney abnormalities, the repair process can lead to fibrosis, which can facilitate progression to chronic kidney disease. Epidemiological studies now show that patients who have had acute kidney injury have a marked increase in their risk for the development of end-stage renal disease. Recent data have redefined the role of the surviving epithelial cells in fibrosis and attribute myofibroblast expansion to perivascular and interstitial fibroblasts. After severe injury, the proximal tubule cellular response is impaired with its proliferative response altered due to cell cycle arrest at the G2/M phase of the cell cycle, resulting in generation of profibrotic factors including cytokines, growth factors and matrix proteins.
肾脏受损后具有自我修复能力。轻度损伤时，这种修复可使肾脏恢复到与正常状态难以区分的结构和功能状态。然而，当修复较为严重或叠加在基线肾脏异常之上时，修复过程会导致纤维化，进而促进向慢性肾脏病的进展。流行病学研究表明，急性肾损伤患者发展为终末期肾病的风险显著增加。近期数据重新定义了存活上皮细胞在纤维化中的作用，并将肌成纤维细胞的扩张归因于血管周围和成纤维细胞。严重损伤后，近端小管细胞反应受损，其增殖反应因细胞周期停滞在G2/M期而改变，导致包括细胞因子、生长因子和基质蛋白在内的促纤维化因子生成。
