Cited by 95Acute Kidney Injury ResearchSepsis Diagnosis and TreatmentChemotherapy-induced organ toxicity mitigation

Gut–kidney crosstalk in septic acute kidney injury

Open access
Zhang, Jingxiao, Ankawi, Ghada, Sun, Jian, Digvijay, Kumar, Yin, Yongjie, Rosner, Mitchell H., Ronco, Claudio·2018·Critical Care

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.

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Crossref · 10.1186/s13054-018-2040-y

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  • Gut-derived inflammatory mediators and endotoxins entering the bloodstream may exacerbate renal injury.

    “Gut-derived inflammatory mediators and endotoxins that enter the bloodstream may exacerbate renal injury [31,32].”

    From Gastrointestinal function and nutritional interventions in septic shock (2025) · cites this paper as [32]

    The Background (page unavailable) says gut-derived bacteria and toxins may enter systemic circulation, amplify inflammation, and potentiate acute kidney injury. The paper also mentions intestinal endotoxin production, but does not specifically say that gut-derived inflammatory mediators enter the bloodstream; it describes systemic inflammation arising after gut-barrier disruption. (LLM, conf=0.78)

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Authors
Zhang, J., Ankawi, G., Sun, J., Digvijay, K., Yin, Y., Rosner, M. H., & Ronco, C.
Affiliations
  • Jilin University (CN)
  • King Abdulaziz University (SA)
  • Sir Ganga Ram Hospital (IN)
  • University of Virginia Health System (US)
  • Ospedale San Bortolo (IT)
Corresponding author
Yin, Yongjie
Venue
Critical Care
Published
2018-05-03
Volume
22
Issue
1
Pages
117-117
ISSN
1364-8535 (ISSN-L)
OpenAlex
W2806389041
Cited by
95
References
63
Citations by year
2026: 16 · 2025: 13 · 2024: 10 · 2023: 21 · 2022: 14 · 2021: 7 · 2020: 10 · 2019: 3 · 2018: 1
FWCI
0.90
Type
journal article
Language
en
Open access
Locations
  • Critical Care (publishedVersion, cc-by)
  • Europe PMC (PubMed Central) (publishedVersion, other-oa)
  • PubMed Central (publishedVersion, cc-by)
  • PubMed (publishedVersion)
  • DOAJ (DOAJ: Directory of Open Access Journals) (submittedVersion)
Topics
  • Health Sciences › Medicine › Nephrology › Acute Kidney Injury Research
  • Health Sciences › Medicine › Epidemiology › Sepsis Diagnosis and Treatment
  • Health Sciences › Medicine › Pathology and Forensic Medicine › Chemotherapy-induced organ toxicity mitigation
Keywords
sepsis-associated acute kidney injury, sepsis, intestinal barrier dysfunction, microbial translocation, gut microbiota, systemic inflammation, inflammatory mediators, metabolic homeostasis, intestinal injury
MeSH terms
Humans, Intensive Care Units, Kidney, Sepsis, Gastrointestinal Tract, Acute Kidney Injury, Microbiota

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