Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
2
pubmed:dateCreated
2004-7-15
pubmed:abstractText
Ischemic acute renal failure (ARF) is increasingly recognized as involving a complex cascade of mechanisms with both acute and chronic consequences. Attention to nontraditional mediators of ARF such as inflammatory pathways and microvascular events has yielded new paradigms and avenues of research. The initiation phase of renal ischemia/reperfusion (I/R) injury damage involves microvascular hemodynamic changes characterized by red blood cell sludging with platelets and leukocytes. Blocking leukocyte-endothelial interactions has yielded significant protection from renal I/R injury in experimental models. However, experiments focusing on the role of the neutrophil have led to a modest expectation of its role in ARF. Recent studies have found that T cells directly mediate renal injury in experimental I/R injury. The CD4+ T cell, working both via interferon-gamma (IFN-gamma) and costimulatory molecules appears to be an important modulator of ARF. The B cell has recently been implicated in ARF. Little is known about the role for the macrophage. Finally, resident kidney cells likely contribute to the inflammatory pathogenesis of I/R damage and protection/repair, but how, and to what extent they are involved is not known. New tools to modulate inflammatory cells, particularly mononuclear leukocytes, hold promise for clinical trials in ARF.
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:status
MEDLINE
pubmed:month
Aug
pubmed:issn
0085-2538
pubmed:author
pubmed:issnType
Print
pubmed:volume
66
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
486-91
pubmed:dateRevised
2010-11-18
pubmed:meshHeading
pubmed:year
2004
pubmed:articleTitle
Inflammatory cells in ischemic acute renal failure.
pubmed:affiliation
Renal Divisions, Thomas Jefferson University Hospital, Philadelphia, Pennsylvania, USA.
pubmed:publicationType
Journal Article, Research Support, U.S. Gov't, P.H.S., Review, Research Support, Non-U.S. Gov't