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Am J Physiol Renal Physiol 267: F1052-F1058, 1994;
0363-6127/94 $5.00
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AJP - Renal Physiology, Vol 267, Issue 6 1052-F1058, Copyright © 1994 by American Physiological Society

ARTICLES

Role of CD11a and CD11b in ischemic acute renal failure in rats

H. Rabb, C. C. Mendiola, J. Dietz, S. R. Saba, T. B. Issekutz, F. Abanilla, J. V. Bonventre and G. Ramirez
Department of Internal Medicine, University of South Florida.

Leukocytes, particularly neutrophils, have been implicated in ischemic-reperfusion organ injury (IRI). However, their role in kidney IRI is controversial. Leukocytes express the adhesion molecules CD11/CD18 on their surface, which mediate many functions that can lead to tissue damage. To determine the role of CD11a and CD11b in IRI in the kidney, uninephrectomized Sprague-Dawley rats were pretreated with monoclonal antibodies (MAbs) directed against CD11a and CD11b or control MAbs. The serum creatinine (SCr), complete blood count, and kidney histopathological damage scores (PDS) (scale: 0-4) were assessed prior to and 24 h after 60 min of ischemia. Mean SCr 24 h after ischemia was significantly decreased in the anti-CD11a- and -CD11b-treated group compared with the control MAb-treated group (2.5 +/- 0.3 mg/dl vs. 3.4 +/- 0.2 mg/dl, P < 0.05). PDS were also reduced in the CD11a and CD11b group compared with controls (2.7 +/- 0.2 vs. 3.5 +/- 0.1, P < 0.001). These data show that the CD11/CD18 leukocyte adhesion pathway plays a role in mediating ischemic acute renal failure in rats.


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