Sheerin N S, Sacks S H
Department of Renal Medicine and Transplantation, The Guy's, King's College and St Thomas' Hospitals' Medical and Dental School, Guy' Hospital, London, UK.
Kidney Blood Press Res. 1999;22(1-2):47-52. doi: 10.1159/000025908.
Tubulointerstitial injury is seen in some patients with glomerular proteinuria and when present is a poor prognostic indicator. However, the mechanism by which proteinuria results in tubular and interstitial damage is unknown. Activation of the complement system has been implicated in many forms of tissue injury, including immune-mediated renal disease. Immunohistochemical studies suggest that complement is deposited on the tubular epithelium in proteinuric states raising the possibility that complement activation may contribute to tubular injury. In this review, we discuss how complement proteins reach the tubular epithelium and why the complement system is activated at this site. We also discuss the effects this may have on tubular cells and how this could result in progressive interstitial disease. The possibility that complement inhibition may reduce progression of tubulointerstitial injury is also considered.
在一些肾小球性蛋白尿患者中可见肾小管间质损伤，一旦出现则是预后不良的指标。然而，蛋白尿导致肾小管和间质损伤的机制尚不清楚。补体系统的激活与多种形式的组织损伤有关，包括免疫介导的肾脏疾病。免疫组织化学研究表明，在蛋白尿状态下补体沉积在肾小管上皮细胞上，这增加了补体激活可能导致肾小管损伤的可能性。在这篇综述中，我们讨论补体蛋白如何到达肾小管上皮细胞以及补体系统在该部位被激活的原因。我们还讨论了这可能对肾小管细胞产生的影响以及这如何导致进行性间质疾病。补体抑制可能减少肾小管间质损伤进展的可能性也在考虑之中。
