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LEUCOCYTE ADHESION MOLECULES IN ISCHAEMIC RENAL INJURY: KIDNEY SPECIFIC PARADIGMS?
Author(s) -
Rabb Hamid,
Postler Gilbert
Publication year - 1998
Publication title -
clinical and experimental pharmacology and physiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.752
H-Index - 103
eISSN - 1440-1681
pISSN - 0305-1870
DOI - 10.1111/j.1440-1681.1998.t01-1-.x
Subject(s) - selectin , cell adhesion molecule , cd18 , kidney , integrin , intercellular adhesion molecule 1 , medicine , acute kidney injury , microbiology and biotechnology , immunology , biology , receptor
1. Renal ischaemic–reperfusion injury (IRI) is an important cause of acute renal failure in native kidneys and in allografts. 2. Leucocyte adhesion molecules CD11/CD18, intercellular adhesion molecule‐1 and selectins mediate cardiac, skin and muscle IRI in experimental models and recent studies have begun to evaluate their role in renal IRI. 3. The CD11/CD18 has been shown to mediate renal IRI in rat models. 4. Intercellular adhesion molecule‐1 has a more prominent role in mediating renal IRI than CD11/CD18 in both rat and mouse models. Blockade of both pathways together appears to provide synergistic protection. 5. Unlike in heart and muscle, L‐selectin does not appear to mediate leucocyte recruitment to postischaemic kidney or tubular damage. 6. Leucocyte adhesion molecules may mediate renal IRI by mechanisms other than simply leucocyte migration, such as signal transduction and cell transport. Presented at the Experimental Biology Symposium on the Role of Integrins in Acute Renal Failure, New Orleans, Louisiana, USA, 1997.