| Organ crosstalk: the role of the kidney. | |
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MedLine Citation:
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PMID: 19851101 Owner: NLM Status: MEDLINE |
Abstract/OtherAbstract:
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PURPOSE OF REVIEW: Acute kidney injury (AKI) continues to contribute significantly to morbidity and mortality in the ICU setting, especially when associated with distant organ dysfunction. There is increasing evidence that AKI directly contributes to organ dysfunction in lung, brain, liver, heart and other organs. This review will examine our current understanding of the deleterious organ crosstalk in the critically ill, which can provide a framework for developing novel therapeutics. RECENT FINDINGS: The majority of studies correlating AKI with distant organ dysfunction have demonstrated the pathophysiological importance of proinflammatory and proapoptotic pathways as well as oxidative stress and reactive oxygen species (ROS) production. Leukocyte activation and infiltration, changes in levels of soluble factors such as cytokines and chemokines, and regulation of cell death in extra-renal organs are potentially important mechanisms by which AKI modulates multiorgan dysfunction. SUMMARY: There is increasing knowledge of AKI and deleterious interorgan crosstalk that arises, at least in part, due to the imbalance of immune, inflammatory, and soluble mediator metabolism that attends severe insults to the kidney. Further studies can build on these new mechanistic observations to develop strategies to improve outcomes in the critically ill patient. |
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Authors:
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Xiang Li; Heitham T Hassoun; Rachel Santora; Hamid Rabb |
Publication Detail:
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Type: Journal Article; Research Support, N.I.H., Extramural; Review |
Journal Detail:
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Title: Current opinion in critical care Volume: 15 ISSN: 1531-7072 ISO Abbreviation: Curr Opin Crit Care Publication Date: 2009 Dec |
Date Detail:
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Created Date: 2009-11-10 Completed Date: 2010-01-28 Revised Date: 2011-05-13 |
Medline Journal Info:
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Nlm Unique ID: 9504454 Medline TA: Curr Opin Crit Care Country: United States |
Other Details:
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Languages: eng Pagination: 481-7 Citation Subset: IM |
Affiliation:
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Department of Medicine, Johns Hopkins University School of Medicine, Baltimore, Maryland, USA. |
Export Citation:
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| MeSH Terms | |
Descriptor/Qualifier:
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Acute Kidney Injury
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complications,
metabolism,
physiopathology* Humans Inflammation / physiopathology Ischemia / physiopathology Multiple Organ Failure / metabolism, physiopathology* |
| Grant Support | |
ID/Acronym/Agency:
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K08 HL089181/HL/NHLBI NIH HHS; K08 HL089181-02/HL/NHLBI NIH HHS; P50 HL073944/HL/NHLBI NIH HHS; R01 DK54770/DK/NIDDK NIH HHS |
From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine
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