Abstract
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.
Original language | English (US) |
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Pages (from-to) | 286-291 |
Number of pages | 6 |
Journal | Clinical and Experimental Pharmacology and Physiology |
Volume | 25 |
Issue number | 3-4 |
DOIs | |
State | Published - Jan 1 1998 |
Externally published | Yes |
Keywords
- Cell adhesion
- Integrins
- Ischaemia
- Kidney
- Leucocytes
- Reperfusion
- Selectins
ASJC Scopus subject areas
- Physiology
- Pharmacology
- Physiology (medical)