Endothelin in the urine of children with the hemolytic uremic syndrome.
Endothelin in the urine of children with the hemolytic uremic syndrome.
复制标题
溶血性尿毒症综合征儿童尿液中的内皮素。
DOI：
10.1542/peds.88.5.1063
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发表时间：
1991
期刊：
影响因子：
8
通讯作者：
M. Mitchell
中科院分区：
文献类型：
--
作者：
R. Siegler;S. Edwin;R. Christofferson;M. Mitchell
经典型儿童溶血尿毒综合征（HUS）的致病级联反应导致急性肾功能衰竭和高血压，其可能是由肾血管内皮细胞损伤引发的。多系统参与经常发生，显然是广泛的内皮细胞扰动的结果。有证据表明，某些产志贺菌的肠道微生物（如大肠杆菌0157：H7）产生的循环志贺样毒素（verotoxins）可导致内皮细胞损伤。血小板和凝血级联激活可能继发于肾微血管内随后的血小板-纤维蛋白沉积。然而，肾活检标本，往往未能显示足够的结构损伤，以解释严重的少尿肾功能衰竭，往往发生在综合征。
The pathogenic cascade leading to acute renal failure and hypertension in classic childhood hemolytic uremic syndrome (HUS) presumably is initiated by injury to the renal vascular endothelial cells. Multisystem involvement often occurs, apparently as a consequence of widespread endothelial cell perturbation. There is evidence that endothelial cell injury can be caused by circulating Shiga-like toxins (verotoxins) produced by certain diarrhea-producing enteric organisms (eg, Escherichia coli 0157:H7). Platelet and coagulation cascade activation probably occur secondarily with subsequent platelet-fibrin deposition within the renal microvasculature. Kidney biopsy specimens, however, often fail to show structural damage sufficient to account for the severe oliguric renal failure that often occurs in the syndrome.