Evidence map›Paper›PMID 18309004›Full record

ReviewClinical journal of the American Society of Nephrology : CJASN2008

Late kidney allograft loss: what we know about it, and what we can do about it.

Anthony M Jevnikar, Roslyn B Mannon

Abstract readReview
In one paragraph

Review in Clinical journal of the American Society of Nephrology : CJASN, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 43 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
43citing papers in PubMed, 1 pooled it
5.2field-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

43 citing papers in PubMed, 1 synthesis or guideline pooled it, 116 citations in OpenAlex.

  1. Pooled it
  2. Correction of postkidney transplant anemia reduces progression of allograft nephropathy.Journal of the American Society of Nephrology : JASN · 2012
    Trial
  3. Review
  4. Late Allograft Loss and Contemporary Cardiorenal Metabolic Therapies.Journal of the American Society of Nephrology : JASN · 2025
    Review
  5. Review
  6. Article
  7. Rationale for Surrogate Endpoints and Conditional Marketing Authorization of New Therapies for Kidney Transplantation.Transplant international : official journal of the European Society for Organ Transplantation · 2022
    Review
  8. Article
  9. Article
  10. High levels of dd-cfDNA identify patients with TCMR 1A and borderline allograft rejection at elevated risk of graft injury.American journal of transplantation : official journal of the American Society of Transplantation and the American Society of Transplant Surgeons · 2020
    Article
  11. Article
  12. Article
  13. Article
  14. Article
  15. IL-7 receptor heterogeneity as a mechanism for repertoire change during postdepletional homeostatic proliferation and its relation to costimulation blockade-resistant rejection.American journal of transplantation : official journal of the American Society of Transplantation and the American Society of Transplant Surgeons · 2018
    Article
  16. Article
  17. Effects of DNA Methylation on Progression to Interstitial Fibrosis and Tubular Atrophy in Renal Allograft Biopsies: A Multi-Omics Approach.American journal of transplantation : official journal of the American Society of Transplantation and the American Society of Transplant Surgeons · 2017
    Article
  18. Article
  19. Review
  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

2 authors at 1 institution in 1 country.

Anthony M JevnikarDepartment of Medicine, Lawson Health Research Institute and Robarts Research Institute, London Health Sciences Centre, University of Western Ontario, London, Ontario, Canada.
Roslyn B Mannon
Western University · CA

Funding

Intramural NIH HHS
6 · The paper itself

Abstract

Despite dramatic improvements in immunosuppression, late graft loss after kidney transplantation remains a common and difficult problem. Histologic evaluation may reveal changes related to BK polyomavirus infection, hypertension, or calcineurin inhibitor toxicity, which can help to guide therapy. The designation chronic allograft nephropathy should thus be reserved for biopsies with tubular atrophy and interstitial fibrosis without an apparent cause. Although the cause clearly includes both antigen-dependent and antigen-independent events, the approach remains largely to exclude immune mechanisms. Although this review discusses the potential contribution of antibody to chronic injury, it focuses on the basic elements of kidney injury, the role of parenchymal cells in promoting injury, and the proliferative and inflammatory responses that accompanying injury. Strategies to manage these recipients include close attention to accompanying hypertension, diabetes, and hyperlipidemia, as well as consideration for altering immunosuppression; however, therapies that limit epithelial-to-mesenchymal transition or directly block fibrosis pathways may reduce chronic allograft fibrosis and may prove to be useful. Understanding the basic pathogenesis sufficiently to allow early intervention may finally benefit patients who are at high risk for tubular atrophy and interstitial fibrosis and promote their long-term graft function.

Indexed as

Kidney TransplantationAtrophyDelayed Graft FunctionFibrosisHumansKidneyTransplantation, Homologous

Identifiers

PMID18309004
PMCPMC3152273
OpenAlexW2112251064

What OpenQuestion holds

Textmetadata
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.