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化学诱导的肾小球损伤:基本机制与特定外源性化学物质综述

Chemically induced glomerular injury: a review of basic mechanisms and specific xenobiotics.

作者信息

Robertson J L

机构信息

Department of Biomedical Sciences and Pathobiology, Virginia-Maryland Regional College of Veterinary Medicine, Virginia Polytechnic Institute and State University, Blacksburg 24091, USA.

出版信息

Toxicol Pathol. 1998 Jan-Feb;26(1):64-72. doi: 10.1177/019262339802600109.

Abstract

Contact with many drugs and chemicals can produce glomerular injury. A common sign of such injury is proteinuria. Chemicals and drugs act through diverse mechanisms to produce injury, including direct damage to cellular and membranous glomerular components, as well as to renal vasculature. Several basic pathophysiologic mechanisms, including the "intact nephron hypothesis" and the "hyperfiltration hypothesis," help to explain the mode of toxicity of many chemicals. Furthermore, they provide a means to understand the basis for renal damage and the progression of renal disease once injury has occurred.

摘要

接触多种药物和化学物质会导致肾小球损伤。这种损伤的一个常见迹象是蛋白尿。化学物质和药物通过多种机制造成损伤,包括直接损害肾小球的细胞和膜性成分以及肾血管系统。几种基本的病理生理机制,包括“完整肾单位假说”和“超滤假说”,有助于解释许多化学物质的毒性模式。此外,它们为理解肾损伤的基础以及损伤发生后肾病的进展提供了一种方法。

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