Evidence map›Paper›PMID 29724256›Full record

ReviewCritical care (London, England)2018

Gut-kidney crosstalk in septic acute kidney injury.

Jingxiao Zhang, Ghada Ankawi, Jian Sun, Kumar Digvijay, Yongjie Yin, Mitchell H Rosner, Claudio Ronco

Open access · goldAbstract readReview
In one paragraph

Review in Critical care (London, England), 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 66 papers.

0numbers the graph read from it
0cells of the map it votes in
66citing papers in PubMed
3.3field-weighted citation impact, top 8% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

66 citing papers in PubMed, 85 citations in OpenAlex.

  1. Trial
  2. Indole-3-carboxaldehyde fromGut microbes · 2026
    Article
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  13. Review
  14. Structural-activity relationship ofFrontiers in immunology · 2026
    Review
  15. Review
  16. Microbiota-gut-kidney axis in health and renal disease.International journal of biological sciences · 2026
    Review
  17. Review
  18. Review
  19. Review
  20. Constipation in critically ill adults.World journal of gastrointestinal pathophysiology · 2025
    Review

6 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

7 authors at 5 institutions in 5 countries.

Jingxiao ZhangDepartment of Emergency and Critical Care Medicine, The Second Hospital of Jilin University, Changchun, China.
Ghada AnkawiDepartment of Internal Medicine and Nephrology, King Abdulaziz University, Jeddah, Saudi Arabia.
Jian SunDepartment of Emergency and Critical Care Medicine, The Second Hospital of Jilin University, Changchun, China.
Kumar DigvijayInternational Renal Research Institute of Vicenza (IRRIV), Vicenza, Italy.
Yongjie YinDepartment of Emergency and Critical Care Medicine, The Second Hospital of Jilin University, Changchun, China. yinyongjie2003@sina.cn.
Mitchell H RosnerDivision of Nephrology, University of Virginia Health System, Charlottesville, VA, USA.
Claudio RoncoInternational Renal Research Institute of Vicenza (IRRIV), Vicenza, Italy.
Second Affiliated Hospital of Jilin University · CNInternational Renal Research Institute of Vicenza · ITKing Abdulaziz University · SASir Ganga Ram Hospital · INUniversity of Virginia Health System · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

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.

Indexed as

Acute Kidney InjuryGastrointestinal TractHumansIntensive Care UnitsKidneyMicrobiotaSepsisSepsis, AKI, Septic AKI, Gut–kidney crosstalk, Inflammation

Identifiers

PMID29724256
PMCPMC5934860
OpenAlexW2806389041

What OpenQuestion holds

Textmetadata
LicenceCC BY
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.