Evidence map›Paper›PMID 29466390›Full record

ArticlePloS one2018

The role of complement activation in rhabdomyolysis-induced acute kidney injury.

XuDong Huang, Wei Zhao, LiXia Zhang, XinJun Yang, LiHui Wang, YunShuang Chen, JingHua Wang, Chao Zhang, GuangLi Wu

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.

0numbers the graph read from it
0cells of the map it votes in
10citing papers in PubMed
1.7field-weighted citation impact, top 17% 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

10 citing papers in PubMed, 20 citations in OpenAlex.

  1. Review
  2. Article
  3. Article
  4. Article
  5. Article
  6. Review
  7. Review
  8. Review
  9. Article
  10. Heme Oxygenase 1: A Defensive Mediator in Kidney Diseases.International journal of molecular sciences · 2021
    Review
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

9 authors at 2 institutions in 1 country.

XuDong HuangDepartment of Nephrology, Chinese PLA General Hospital, Beijing, the People's Republic of China.ORCID 0000-0001-8029-1204
Wei ZhaoDepartment of Nephrology, Bethune International Peace Hospital, Shijiazhuang, Hebei Province, the People's Republic of China.
LiXia ZhangDepartment of Nephrology, Bethune International Peace Hospital, Shijiazhuang, Hebei Province, the People's Republic of China.
XinJun YangDepartment of Nephrology, Bethune International Peace Hospital, Shijiazhuang, Hebei Province, the People's Republic of China.
LiHui WangDepartment of Nephrology, Bethune International Peace Hospital, Shijiazhuang, Hebei Province, the People's Republic of China.
YunShuang ChenDepartment of Nephrology, Bethune International Peace Hospital, Shijiazhuang, Hebei Province, the People's Republic of China.
JingHua WangDepartment of Nephrology, Bethune International Peace Hospital, Shijiazhuang, Hebei Province, the People's Republic of China.
Chao ZhangDepartment of Nephrology, Bethune International Peace Hospital, Shijiazhuang, Hebei Province, the People's Republic of China.
GuangLi WuDepartment of Nephrology, Chinese PLA General Hospital, Beijing, the People's Republic of China.
Bethune International Peace Hospital · CNChinese PLA General Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Rhabdomyolysis (RM) may cause kidney damage and results primarily in acute kidney injury (AKI). Complement is implicated in the pathogenesis of renal diseases and ischemia-reperfusion injury (IRI), but the role of complement, especially its activation pathway(s) and its effect in RM-induced AKI, is not clear. This study established a rat model of AKI induced by RM via intramuscular treatment with glycerol. Cobra venom factor (CVF) was administered via tail vein injection to deplete complement 12 h prior to intramuscular injection of glycerol. We found that the complement components, including complement 3 (C3), C1q, MBL-A, factor B(fB), C5a, C5b-9, and CD59, were significantly increased in rat kidneys after intramuscular glycerol administration. However, the levels of serum BUN and Cr, renal tubular injury scores, and the number of TUNEL-positive cells decreased significantly in the CVF+AKI group. These results suggest that complement plays an important role in RM-induced AKI and that complement depletion may improve renal function and decrease renal tissue damage by reducing the inflammatory response and apoptosis.

Indexed as

Complement ActivationDisease Models, AnimalAcute Kidney InjuryAnimalsGlycerolIn Situ Nick-End LabelingMaleRatsRats, Sprague-DawleyReal-Time Polymerase Chain ReactionRhabdomyolysisGlycerol

Identifiers

PMID29466390
PMCPMC5821337
OpenAlexW2790923733

What OpenQuestion holds

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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.