Evidence map›Paper›PMID 24991565›Full record

ReviewBioMed research international2014

The Interplay between inflammation and fibrosis in kidney transplantation.

Irina B Torres, Francesc Moreso, Eduard Sarró, Anna Meseguer, Daniel Serón

Open access · hybridAbstract readReview
In one paragraph

Review in BioMed research international, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.

0numbers the graph read from it
0cells of the map it votes in
29citing papers in PubMed
5.1field-weighted citation impact, top 4% 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

29 citing papers in PubMed, 63 citations in OpenAlex.

  1. Article
  2. Cellular and Molecular Aspects of Chronic Rejection.Results and problems in cell differentiation · 2026
    Review
  3. Noninvasive diagnosis and classification of kidney transplantation rejection byEuropean journal of nuclear medicine and molecular imaging · 2025
    Article
  4. Review
  5. Review
  6. Review
  7. Article
  8. Article
  9. Article
  10. Article
  11. Article
  12. Review
  13. Review
  14. Article
  15. Article
  16. Matrix Metalloproteinases in Diabetic Kidney Disease.Journal of clinical medicine · 2020
    Review
  17. Article
  18. Article
  19. The TGF-Mediators of inflammation · 2018
    Article
  20. Article
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

5 authors at 2 institutions in 1 country.

Irina B TorresNephrology Department, Vall d'Hebron University Hospital, Autonomous University of Barcelona, Passeig Vall d'Hebron 119-129, 08035 Barcelona, Spain.
Francesc MoresoNephrology Department, Vall d'Hebron University Hospital, Autonomous University of Barcelona, Passeig Vall d'Hebron 119-129, 08035 Barcelona, Spain.
Eduard SarróRenal Physiopathology Department, CIBBIM-Nanomedicine, Vall d'Hebron Research Institute, Passeig Vall d'Hebron 119-129, 08035 Barcelona, Spain.
Anna MeseguerRenal Physiopathology Department, CIBBIM-Nanomedicine, Vall d'Hebron Research Institute, Passeig Vall d'Hebron 119-129, 08035 Barcelona, Spain.ORCID 0000-0003-3833-2249
Daniel SerónNephrology Department, Vall d'Hebron University Hospital, Autonomous University of Barcelona, Passeig Vall d'Hebron 119-129, 08035 Barcelona, Spain.
Universitat Autònoma de Barcelona · ESVall d'Hebron Institut de Recerca · ES

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Serial surveillance renal allograft biopsies have shown that early subclinical inflammation constitutes a risk factor for the development of interstitial fibrosis. More recently, it has been observed that persistent inflammation is also associated with fibrosis progression and chronic humoral rejection, two histological conditions associated with poor allograft survival. Treatment of subclinical inflammation with steroid boluses prevents progression of fibrosis and preserves renal function in patients treated with a cyclosporine-based regimen. Subclinical inflammation has been reduced after the introduction of tacrolimus based regimens, and it has been shown that immunosuppressive schedules that are effective in preventing acute rejection and subclinical inflammation may prevent the progression of fibrosis and chronic humoral rejection. On the other hand, minimization protocols are associated with progression of fibrosis, and noncompliance with the immunosuppressive regime constitutes a major risk factor for chronic humoral rejection. Thus, adequate immunosuppressive treatment, avoiding minimization strategies and reinforcing educational actions to prevent noncompliance, is at present an effective approach to combat the progression of fibrosis.

Indexed as

CyclosporineFibrosisGraft RejectionGraft SurvivalHumansImmunosuppressive AgentsInflammationKidney TransplantationTacrolimusCyclosporineImmunosuppressive AgentsTacrolimus

Identifiers

PMID24991565
PMCPMC4065724
OpenAlexW2148348339

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.