Rabb H, O'Meara Y M, Maderna P, Coleman P, Brady H R
Division of Nephrology and Hypertension, University of South Florida, USA.
Kidney Int. 1997 May;51(5):1463-8. doi: 10.1038/ki.1997.200.
Ischemic acute renal failure (ARF) is a common clinical syndrome, associated with high morbidity and mortality, for which there is no specific therapy. Polymorphonuclear neutrophils (PMN) recruited during reperfusion have been implicated as mediators of renal parenchymal injury in ischemic ARF. Leukocyte adhesion molecules appear to facilitate PMN recruitment in this setting. Complementary studies using monoclonal antibodies, antisense oligonucleotides and gene "knock-out" indicate that blockade of CD11/CD18 integrins and intercellular adhesion molecule-1 (ICAM-1) attenuates ARF in some experimental models of renal ischemia. These exciting observations may herald the development of novel anti-adhesion strategies for use in human disease.
缺血性急性肾衰竭(ARF)是一种常见的临床综合征,发病率和死亡率都很高,目前尚无特效治疗方法。再灌注期间募集的多形核中性粒细胞(PMN)被认为是缺血性ARF肾实质损伤的介质。在这种情况下,白细胞粘附分子似乎有助于PMN的募集。使用单克隆抗体、反义寡核苷酸和基因“敲除”的补充研究表明,在一些肾缺血实验模型中,阻断CD11/CD18整合素和细胞间粘附分子-1(ICAM-1)可减轻ARF。这些令人振奋的观察结果可能预示着用于人类疾病的新型抗粘附策略的开发。