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Leukocytes, cell adhesion molecules and ischemic acute renal failure
H Rabb1, Y M O'Meara, P Maderna
1Division of Nephrology and Hypertension, University of South Florida, USA.
Kidney International
|May 1, 1997
Summary
Ischemic acute renal failure (ARF) lacks specific therapies. Blocking leukocyte adhesion molecules like CD11/CD18 and ICAM-1 shows promise in reducing kidney injury in experimental models, potentially leading to new treatments.
Area of Science:
- Nephrology
- Immunology
- Pathophysiology
Background:
- Ischemic acute renal failure (ARF) is a significant clinical syndrome with high morbidity and mortality.
- Polymorphonuclear neutrophils (PMN) are implicated in mediating renal parenchymal injury during ischemic ARF.
- Leukocyte adhesion molecules are crucial for PMN recruitment in this context.
Purpose of the Study:
- To investigate the role of leukocyte adhesion molecules in mediating renal injury during ischemic ARF.
- To evaluate the therapeutic potential of blocking specific adhesion molecules in experimental models of renal ischemia.
Main Methods:
- Utilized experimental models of renal ischemia.
- Employed strategies including monoclonal antibodies, antisense oligonucleotides, and gene "knock-out" to block CD11/CD18 integrins and intercellular adhesion molecule-1 (ICAM-1).
Main Results:
- Blockade of CD11/CD18 integrins and ICAM-1 attenuated renal injury in experimental models of ischemic ARF.
- These findings support the involvement of PMN recruitment via adhesion molecules in ischemic kidney damage.
Conclusions:
- Targeting leukocyte adhesion molecules represents a potential therapeutic strategy for ischemic ARF.
- Further development of anti-adhesion therapies may offer novel treatment options for human ARF.