Evidence map›Paper›PMID 30880546›Full record

ArticleRenal failure2019

Hirudin ameliorates immunoglobulin A nephropathy by inhibition of fibrosis and inflammatory response.

Fei Deng, Jingwei Zhang, Yi Li, Wei Wang, Daqing Hong, Guisen Li, Jing Feng

RetractedOpen access · goldAbstract readRetracted Publication
In one paragraph

Article in Renal failure, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It has been retracted, and should not be counted. Cited by 13 papers.

0numbers the graph read from it
0cells of the map it votes in
13citing papers in PubMed
1.5field-weighted citation impact, top 20% 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

13 citing papers in PubMed, 20 citations in OpenAlex.

  1. Article
  2. Article
  3. Review
  4. Hirudin in the Treatment of Chronic Kidney Disease.Molecules (Basel, Switzerland) · 2024
    Review
  5. Acta pharmaceutica Sinica. B · 2024
    Review
  6. Review
  7. Article
  8. Article
  9. Article
  10. Article
  11. Article
  12. Review
  13. Article
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

7 authors at 2 institutions in 1 country.

Fei Denga Department of Nephrology , Sichuan Academy of Medical Science & Sichuan Provincial People's Hospital , Chengdu , PR China.
Jingwei Zhangb Department of Laboratory Medicine , Chengdu Second People's Hospital , Chengdu , PR China.
Yi Lia Department of Nephrology , Sichuan Academy of Medical Science & Sichuan Provincial People's Hospital , Chengdu , PR China.
Wei Wanga Department of Nephrology , Sichuan Academy of Medical Science & Sichuan Provincial People's Hospital , Chengdu , PR China.
Daqing Honga Department of Nephrology , Sichuan Academy of Medical Science & Sichuan Provincial People's Hospital , Chengdu , PR China.
Guisen Lia Department of Nephrology , Sichuan Academy of Medical Science & Sichuan Provincial People's Hospital , Chengdu , PR China.
Jing Fengc Department of Traditional Chinese Medicine , Sichuan Academy of Medical Science & Sichuan Provincial People's Hospital , Chengdu , PR China.
Sichuan Academy of Medical Sciences & Sichuan Provincial People's Hospital · CNChengdu Second People's Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Immunoglobulin A nephropathy (IgAN) is characterized by mesangial IgA and IgG co-deposition. As the clinical course of IgAN is highly variable, a lot of patients will eventually develop to end-stage renal disease (ESRD) within years. Hirudin, a potent and specific thrombin inhibitor, has been reported to treat IgAN with hematuria, but the mechanism is unclear. Our study aims to explore the potential of hirudin and the underlying mechanism in the treatment of IgAN. The establishment of IgAN model was set up in rats through oral and intravenous immunization with bovine gamma-globulin (BGG). Results suggested that hirudin could reduce the increased level of proteinuria, serum creatinine and urea nitrogen in IgAN models. Besides that, hirudin ameliorated the elevated number of apoptotic bodies and expressions of apoptosis-related proteins (caspase-3 and caspase-9) in IgAN model. The fibrosis indexes (transforming growth factor β-1 (TGF-β1), Collagen-IV (CoI-IV) and Fibronectin-1) of kidney were remarkably suppressed in IgAN rats treated with hirudin compared with IgAN rats with no further treatment. IgAN rats exhibited remarkably increased inflammatory factors (IL-1β, IL-6, and IL-18), while hirudin treatment significantly alleviated these alterations. Moreover, the reduced levels of CD4

Indexed as

AnimalsAntithrombinsCreatinineDisease Models, AnimalFibrosisgamma-GlobulinsGlomerulonephritis, IGAHematuriaHirudinsHirudin TherapyHumansKidneyMaleProteinuriaRatsRats, Sprague-DawleyAntithrombinsCreatininegamma-GlobulinsHirudinsfibrosishirudinImmunoglobulin A nephropathyinflammatory response

Identifiers

PMID30880546
PMCPMC6427573
OpenAlexW2922443711

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.