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蛋白尿作为肾小管间质损伤的介质。

Proteinuria as a mediator of tubulointerstitial injury.

作者信息

Abbate M, Remuzzi G

机构信息

Mario Negri Institute for Pharmacological Research, Azienda Ospedaliera, Ospedali Riuniti di Bergamo, Italy.

出版信息

Kidney Blood Press Res. 1999;22(1-2):37-46. doi: 10.1159/000025907.

DOI:10.1159/000025907
PMID:10352406
Abstract

Proteinuria is one of the most potent risk factors for renal disease progression in patients with glomerular diseases. Studies in disease models have helped to delineate mechanisms leading to renal structural damage due to persistent dysfunction of the glomerular barrier to proteins, even when the primary immune or nonimmune insult to the kidney has ceased. The main focus of this review is the role of the tubular epithelial cell in the induction of interstitial inflammatory and fibrogenic reactions to ultrafiltered proteins. Antiproteinuric drugs (angiotensin-converting enzyme inhibitors, ACEi) while preserving the integrity of the glomerular permselective barrier limit both proteinuria and protein-dependent processes which contribute to tubulointerstitial injury, and in so doing ACEi halt the progression of proteinuric nephropathies toward terminal renal failure.

摘要

蛋白尿是肾小球疾病患者肾脏疾病进展的最主要危险因素之一。疾病模型研究有助于阐明由于肾小球蛋白质屏障持续功能障碍导致肾脏结构损伤的机制,即使对肾脏的原发性免疫或非免疫损伤已经停止。本综述的主要重点是肾小管上皮细胞在对超滤蛋白质诱导间质炎症和纤维化反应中的作用。抗蛋白尿药物(血管紧张素转换酶抑制剂,ACEi)在保持肾小球电荷选择性屏障完整性的同时,限制了蛋白尿和导致肾小管间质损伤的蛋白质依赖性过程,这样一来,ACEi可阻止蛋白尿性肾病向终末期肾衰竭发展。

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Proteinuria as a mediator of tubulointerstitial injury.蛋白尿作为肾小管间质损伤的介质。
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