BackgroundRenal interstitial fibrosis (RIF) is the final common pathway of chronic kidney disease (CKD) to the end stage renal failure (ESRF), characterized with the tubular epithelial cell depletion and expanding of extracelluar matrix (ECM). Tubulointerstitial scarring correlates much better with renal function than glomerular lesions .To prevent the occurrence and progression of RIF is an important content of renal protection.There are a lot of etiopathogenisis for the RIF, and the pathogenesy are very complicated. Modern study reveal that the mechanism of RIF involves the tubulointerstitial cell damage and ECM metabolism abnormity, including the tubular epithelial deletion and phenotype transdifferentiation, interstitial fibroblast proliferation and activation, pro-fibrous cellular factor's production, abnormity of cell apoptosis, ECM over synthesis, ECM degradation obstacle, and so on. These factors above interact between each other, compose a complicate network. It's so complicate that the pathogenesis of RIF is not very clear.According the mechanism of RIF, in modern medicine people cure RIF through anti cell damage and anti-fibrous factor, and has achieved some good performance. |