Evidence map›Paper›PMID 25320909›Full record

ReviewCurrent opinion in critical care2014

Sepsis-induced acute kidney injury revisited: pathophysiology, prevention and future therapies.

Alexander Zarbock, Hernando Gomez, John A Kellum

Open access · greenAbstract readReview
PubMed Full text at PMC Publisher
In one paragraph

Review in Current opinion in critical care, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 214 papers, 5 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
214citing papers in PubMed, 5 pooled it
8.3field-weighted citation impact, top 2% 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

214 citing papers in PubMed, 5 syntheses or guidelines pooled it, 343 citations in OpenAlex.

  1. Pooled it
  2. Pooled it
  3. Pooled it
  4. Pooled it
  5. Pooled it
  6. Trial
  7. Trial
  8. Review
  9. Article
  10. Article
  11. Kidney Support Therapy: Recent Advances.Indian journal of pediatrics · 2026
    Review
  12. Article
  13. Article
  14. Article
  15. Article
  16. Continuous renal replacement therapy in acute liver failure.World journal of critical care medicine · 2026
    Review
  17. Review
  18. Observational
  19. Article
  20. Review

154 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

3 authors at 1 institution in 1 country.

Alexander ZarbockaDepartment of Anesthesiology, Intensive Care and Pain Medicine, University of Münster, Münster, Germany bCenter for Critical Care Nephrology cDepartment of Critical Care Medicine, CRISMA Center, University of Pittsburgh, Pennsylvania, USA.
Hernando Gomez
John A Kellum
University of Pittsburgh · US

Funding

Pittsburgh Career Development Program in Emergency Medicine ResearchK12HL109068 · NHLBI · UNIVERSITY OF PITTSBURGH AT PITTSBURGH · PI CALLAWAY, CLIFTON W., YEALY, DONALD M · 2011 to 2015
$3.1M
Biological Markers of Recovery for the KidneyR01DK070910 · NIDDK · UNIVERSITY OF PITTSBURGH AT PITTSBURGH · PI KELLUM, JOHN A · 2006 to 2010
$1.8M
NHLBI NIH HHS 1K12HL109068-02NHLBI NIH HHS K12 HL109068NIDDK NIH HHS R01 DK070910
6 · The paper itself

Abstract

purpose of reviewAcute kidney injury (AKI) is a common complication in critically ill patients and is associated with increased morbidity and mortality. Sepsis is the most common cause of AKI. Considerable evidence now suggests that the pathogenic mechanisms of sepsis-induced AKI are different from those seen in other causes of AKI. This review focuses on the recent advances in this area and discusses possible therapeutic interventions that might derive from these new insights into the pathogenesis of sepsis-induced AKI. RECENT

findingsThe traditional paradigm that sepsis-induced AKI arises from ischemia has been challenged by recent evidence that total renal blood flow in is not universally impaired during sepsis, and AKI can develop in the presence of normal or even increased renal blood flow. Animal and human studies suggest that adaptive responses of tubular epithelial cells to injurious signals are responsible for renal dysfunction. Simultaneously occurring renal inflammation and microcirculatory dysfunction further amplify these mechanisms. SUMMARY: An understanding of the pathologic mechanisms of sepsis-induced AKI emphasizes the important role of maladaptive responses to the septic insult. Preventive and therapeutic measures should be based on counteracting these maladaptive responses of tubular epithelial cells, inflammation, and microvascular dysfunction.

Indexed as

Acute Kidney InjuryHumansKidneyMicrocirculationSepsis

Identifiers

PMID25320909
PMCPMC4495653
OpenAlexW2015213851

What OpenQuestion holds

Textmetadata
LicenceTDM
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.