el Nahas A M, Muchaneta-Kubara E C, Essawy M, Soylemezoglu O
Sheffield Kidney Institute, Northern General Hospital Trust, U.K.
Int J Biochem Cell Biol. 1997 Jan;29(1):55-62. doi: 10.1016/s1357-2725(96)00119-7.
The progression of chronic renal failure is characterised histologically by glomerulosclerosis, tubulointerstitial fibrosis and vascular sclerosis. Recent research has identified common mechanisms underlying these fibrotic processes. In particular, the scarring process within the glomeruli and the tubulointerstitium involves the infiltration by inflammatory cells including monocytes, the activation of intrinsic renal cells as well as interactions between infiltrating and resident cells. These interactions depend, to a large extent, on the release by these cells of chemokines, cytokines and growth factors. These factors are in turn involved in the induction of cellular proliferation within the kidney and the stimulation of the synthesis and deposition of extracellular collagenous matrix. Fibrosis is believed to result from excessive synthesis of extracellular matrix and a concommitant decrease in its breakdown. This fibrotic process resulting in end stage renal insufficiency bears strong similarities to that taking place within cirrhotic livers or fibrotic lungs. The new insights in our understanding of renal fibrosis have opened the way to new interventions aimed at its prevention. This may ultimately slow the progression of chronic renal insufficiency and decrease the number of patients requiring dialysis replacement therapy.
慢性肾衰竭的进展在组织学上的特征为肾小球硬化、肾小管间质纤维化和血管硬化。最近的研究已经确定了这些纤维化过程的共同机制。特别是，肾小球和肾小管间质内的瘢痕形成过程涉及包括单核细胞在内的炎性细胞浸润、肾固有细胞的激活以及浸润细胞与驻留细胞之间的相互作用。这些相互作用在很大程度上取决于这些细胞释放趋化因子、细胞因子和生长因子。这些因子反过来又参与诱导肾脏内的细胞增殖以及刺激细胞外胶原基质的合成和沉积。纤维化被认为是由于细胞外基质过度合成以及其降解同时减少所致。这种导致终末期肾功能不全的纤维化过程与肝硬化肝脏或纤维化肺内发生的过程极为相似。我们对肾纤维化认识的新见解为旨在预防肾纤维化的新干预措施开辟了道路。这最终可能会减缓慢性肾功能不全的进展，并减少需要透析替代治疗的患者数量。
