Department of Dentistry-Orthodontics and Craniofacial Biology, Radboud Institute for Molecular Life Sciences, Radboud University Medical Center, Nijmegen, the Netherlands.
Department of Pediatric Nephrology, Radboud Institute for Molecular Life Sciences, Amalia Children's Hospital, Radboud University Medical Center, Nijmegen, the Netherlands.
Kidney Int. 2022 Jun;101(6):1107-1109. doi: 10.1016/j.kint.2022.02.026.
Hemolytic uremic syndrome can be initiated by Escherichia coli infections (Shiga-toxin-producing enterohemorrhagic Escherichia coli hemolytic uremic syndrome). When hemoglobin and heme released from ruptured erythrocytes interact with the kidney cells, this can result in platelet activation, vascular inflammation and occlusion, and kidney injury. Pirschel et al. now report that in the absence of protective mechanisms against free hemoglobin and heme, heme-induced kidney injury can be exacerbated. Therapeutic strategies should therefore also target heme-mediated deleterious effects in (severely ill) patients with Shiga-toxin-producing enterohemorrhagic Escherichia coli hemolytic uremic syndrome.
溶血尿毒综合征可由大肠杆菌感染（产志贺毒素的肠出血性大肠杆菌溶血尿毒综合征）引发。当从破裂的红细胞中释放的血红蛋白和血红素与肾细胞相互作用时，这可能导致血小板激活、血管炎症和闭塞以及肾损伤。Pirschel 等人现在报告说，在缺乏针对游离血红蛋白和血红素的保护机制的情况下，血红素诱导的肾损伤可能会加剧。因此，在（重病）产志贺毒素的肠出血性大肠杆菌溶血尿毒综合征患者中，治疗策略也应针对血红素介导的有害作用。
