Title |
Gut–kidney crosstalk in septic acute kidney injury
|
---|---|
Published in |
Critical Care, May 2018
|
DOI | 10.1186/s13054-018-2040-y |
Pubmed ID | |
Authors |
Jingxiao Zhang, Ghada Ankawi, Jian Sun, Kumar Digvijay, Yongjie Yin, Mitchell H. Rosner, Claudio Ronco |
Abstract |
Sepsis is the leading cause of acute kidney injury (AKI) in the intensive care unit (ICU). Septic AKI is a complex and multifactorial process that is incompletely understood. During sepsis, the disruption of the mucus membrane barrier, a shift in intestinal microbial flora, and microbial translocation may lead to systemic inflammation, which further alters host immune and metabolic homeostasis. This altered homeostasis may promote and potentiate the development of AKI. As part of this vicious cycle, when AKI develops, the clearance of inflammatory mediators and metabolic products is decreased. This will lead to further gut injury and breakdown in mucous membrane barriers. Thus, changes in the gut during sepsis can initiate and propagate septic AKI. This deleterious gut-kidney crosstalk may be a potential target for therapeutic maneuvers. This review analyses the underlying mechanisms in gut-kidney crosstalk in septic AKI. |
X Demographics
Geographical breakdown
Country | Count | As % |
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Mexico | 8 | 12% |
United Kingdom | 6 | 9% |
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Sweden | 2 | 3% |
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Belgium | 1 | 2% |
Malaysia | 1 | 2% |
Australia | 1 | 2% |
Hungary | 1 | 2% |
Other | 5 | 8% |
Unknown | 33 | 51% |
Demographic breakdown
Type | Count | As % |
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Members of the public | 45 | 69% |
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Scientists | 6 | 9% |
Science communicators (journalists, bloggers, editors) | 2 | 3% |
Mendeley readers
Geographical breakdown
Country | Count | As % |
---|---|---|
Unknown | 90 | 100% |
Demographic breakdown
Readers by professional status | Count | As % |
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Researcher | 12 | 13% |
Other | 12 | 13% |
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Student > Ph. D. Student | 8 | 9% |
Student > Bachelor | 6 | 7% |
Other | 19 | 21% |
Unknown | 23 | 26% |
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Other | 11 | 12% |
Unknown | 27 | 30% |