Division of Hygiene and Medical Microbiology, Innsbruck Medical University, Innsbruck, Austria.
Semin Thromb Hemost. 2010 Sep;36(6):620-4. doi: 10.1055/s-0030-1262883. Epub 2010 Sep 23.
Hemolytic uremic syndrome (HUS) is a severe disease characterized by the clinical triad of hemolytic anemia, thrombocytopenia, and acute renal failure. HUS exists in two forms: the atypical diarrhea-negative HUS, which is often associated with complement disorders, and the more frequent diarrheal-associated typical HUS, which is caused by infections with enterohemorrhagic ESCHERICHIA COLI. The virulence factors of the latter have been studied well, and Shiga toxin (Stx)2 is reported to represent the most important one. In contrast, risk factors on the host side have not been intensively studied until recently: Complement activation products have been detected in the serum and plasma of HUS patients, and an in vitro study could show that Stx2 not only damages the kidney directly but also indirectly via complement, in two ways. First, it activates complement, and second, it delays the functions of its control protein factor H on the cell surface, both known to damage the kidney.
溶血性尿毒症综合征（HUS）是一种严重的疾病，其特征为溶血性贫血、血小板减少和急性肾衰竭三联征。HUS 存在两种形式：非典型腹泻阴性 HUS，常与补体紊乱有关；以及更常见的腹泻相关典型 HUS，由产志贺样毒素（Stx）的肠出血性大肠杆菌感染引起。后者的毒力因子已得到充分研究，据报道，志贺毒素 2（Stx2）是最重要的一种。相比之下，直到最近宿主方面的危险因素才得到深入研究：HUS 患者的血清和血浆中检测到补体激活产物，体外研究表明 Stx2 不仅直接损害肾脏，还通过补体间接损害肾脏，其机制有两种。首先，它激活补体，其次，它延迟其控制蛋白因子 H 在细胞表面的功能，这两者都已知会损害肾脏。
