Weinhard Jules, Serre Justine, Frère Perrine, Adam Clovis, Lafargue Marie Camille, Buob David, Rafat Cédric
Service de Néphrologie, Dialyse, Aphérèses et Transplantation Rénale, CHU Grenoble Alpes, La Tronche, France.
Soins Intensifs Néphrologiques et Rein Aigu, Hôpital Tenon, AP-HP, Paris, France.
Kidney Med. 2024 Dec 24;7(3):100952. doi: 10.1016/j.xkme.2024.100952. eCollection 2025 Mar.
-related kidney toxicity is poorly documented and remains to be elucidated. Herein, we describe the case of a 43-year old patient who presented with severe liver failure following the ingestion of . Although liver injury subsided following the administration of N-acetyl cystein and silibinin, the patient subsequently developed KDIGO stage 3 acute kidney injury. Histopathological examination of the kidney displayed moderate tubular injury characterized by dilated tubular lumens and flattening of the tubular epithelium on optic microscopy. Electron microscopy showed mitochondrial changes including swelling and decreased number of cristae. Immunofluorescence for the key mitochondrial protein TOM20 found significantly decreased expression compared with ischemic acute tubular injury. Despite these changes, histoenzymology showed preserved succinate cytochrome c oxidase (COX) expression, suggesting that mitochondrial complex IV function was maintained. Our findings suggest that elicits acute tubular injury via mitochondrial damage, possibly through a pathway that spares COX function.
相关的肾毒性记录较少，仍有待阐明。在此，我们描述了一名43岁患者的病例，该患者在摄入……后出现严重肝功能衰竭。尽管在给予N - 乙酰半胱氨酸和水飞蓟宾后肝损伤消退，但患者随后发展为KDIGO 3期急性肾损伤。肾脏的组织病理学检查显示中度肾小管损伤，光学显微镜下表现为肾小管腔扩张和肾小管上皮扁平。电子显微镜显示线粒体变化，包括肿胀和嵴数量减少。关键线粒体蛋白TOM20的免疫荧光显示与缺血性急性肾小管损伤相比表达显著降低。尽管有这些变化，组织酶学显示琥珀酸细胞色素c氧化酶（COX）表达保留，表明线粒体复合物IV功能得以维持。我们的研究结果表明……通过线粒体损伤引发急性肾小管损伤，可能是通过一条不影响COX功能的途径。
