目的　进一步探讨环孢素A(CsA)肾毒性的发病机制 ,并为临床防治CsA所致急性肾损伤提供依据。方法　采用生化、免疫组化和透射电镜方法。结果　CsA使肾皮质内皮素 - 1(ET - 1)水平增高 ,肾组织中超氧化物歧化酶 (SOD)活力下降 ,丙二醛 (MDA)含量增多 ,肾小管上皮细胞Na+ ,K+ -ATP酶活性降低 ,并造成肾、肝、肺组织结构破坏 ,还原性谷胱甘肽 (TAD)可使上述病变减轻。结论　血流动力学改变和脂质过氧化损伤是CsA致急性肾损伤的重要原因 ,TAD有良好的保护作用。 Objective To further explore the pathogenesis of cyclosporin A (CsA) nephrotoxicity and provide the basis for clinical prevention and treatment of acute renal injury induced by CsA. Methods Biochemical, immunohistochemical and transmission electron microscopy methods. Results CsA increased the level of endothelin - 1 (ET - 1) in renal cortex, decreased the activity of superoxide dismutase (SOD) and the content of malondialdehyde (MDA) in renal tissue, and increased the activity of Na +, K + -ATPase in renal tubular epithelial cells Reduce, and cause kidney, liver and lung tissue damage, reduced glutathione (TAD) can reduce the above lesions. Conclusions Hemodynamic changes and lipid peroxidation injury are the important causes of CsA-induced acute kidney injury. TAD has a good protective effect.