TUBULOINTERSTITIAL LESIONS MEDIATE RENAL DAMAGE IN ADRIAMYCIN GLOMERULOPATHY
TUBULOINTERSTITIAL LESIONS MEDIATE RENAL DAMAGE IN ADRIAMYCIN GLOMERULOPATHY
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DOI：
10.1038/ki.1986.212
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发表时间：
1986-10-01
影响因子：
19.6
通讯作者：
REMUZZI, G
中科院分区：
文献类型：
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作者：
BERTANI, T;CUTILLO, F;REMUZZI, G
本研究旨在探讨蛋白尿、局灶性硬化和肾小管间质改变在实验性肾病肾损害演变中的关系。我们利用加速单侧模型阿霉素（ADR）肾病的特点是形态学变化更严重，比经典模型。ADR引起的肾小球病变的第一个事件是上皮细胞损伤和蛋白尿。随后，在远端水平形成管状铸件。病例形成先于间质性损伤的发展，这是由肾小管阻塞和肾小管基底膜（TBM）破裂决定的，这反过来又促进了间质性炎症反应。尽管在长期大量蛋白尿后观察到肾小管间质损伤的严重性，但局灶节段性肾小球硬化（FSG）的发生率非常低。本研究的结果表明，慢性蛋白尿不一定伴随着局灶性硬化的发展。肾小管间质病变似乎是该模型中肾损害进展的最重要决定因素。
The present study was designed to investigate the relationship between proteinuria, focal sclerosis, and tubulo-interstitial changes in the evolution of renal damage in experimental nephrosis. We utilized an accelerated unilateral model of adriamycin (ADR) nephrosis characterized by morphological changes more severe than in the classical model. The first events in ADR-induced glomerulopathy were epithelial cell damage and proteinuria. Subsequently, tubular casts were formed at the distal level. The case formation preceded the development of interstitial damage, which was determined by tubular obstruction and breaking of tubular basement membrane (TBM), which in turn promoted an interstitial inflammatory reaction. Despite the severity of tubulo-interstitial damage observed after a long period of heavy proteinuria, the incidence of focal segmental glomerulosclerosis (FSG) was very low. The results of the present study indicate that chronic proteinuria is not necessarily accompanied by the development of focal sclerosis. Tubulo-interstitial lesions appear to be the most important determinant for the progression of renal damage in this model.