Evidence map›Paper›PMID 24700797›Full record

ReviewClinical journal of the American Society of Nephrology : CJASN2014

De novo glomerular diseases after renal transplantation.

Claudio Ponticelli, Gabriella Moroni, Richard J Glassock

Abstract readReview
In one paragraph

Review in Clinical journal of the American Society of Nephrology : CJASN, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.

0numbers the graph read from it
0cells of the map it votes in
25citing papers in PubMed
3.9field-weighted citation impact, top 6% 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

25 citing papers in PubMed, 60 citations in OpenAlex.

  1. Review
  2. Article
  3. Case report: Early onsetFrontiers in pediatrics · 2023
    Article
  4. Article
  5. Review
  6. IsWorld journal of transplantation · 2022
    Article
  7. Article
  8. Review
  9. Review
  10. Review
  11. De novo pauci-immune glomerulonephritis in renal allografts.Modern pathology : an official journal of the United States and Canadian Academy of Pathology, Inc · 2020
    Article
  12. Article
  13. Article
  14. Article
  15. Article
  16. Recurrent andFrontiers in immunology · 2019
    Review
  17. World journal of transplantation · 2017
    Review
  18. Article
  19. Targeting mTOR Signaling Can Prevent the Progression of FSGS.Journal of the American Society of Nephrology : JASN · 2017
    Article
  20. Primary Membranous Nephropathy.Clinical journal of the American Society of Nephrology : CJASN · 2017
    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

3 authors at 3 institutions in 2 countries.

Claudio PonticelliDivision of Nephrology, Humanitas Scientific Institute, Rozzano, Milan, Italy; ponticelli.claudio@gmail.com.
Gabriella MoroniDivision of Nephrology, Fondazione Ca' Granda Ospedale Maggiore Istituto Scientifico, Milan, Italy; and.
Richard J GlassockDepartment of Medicine, Geffen School of Medicine at the University of California at Los Angeles, Laguna Niguel, California.
Fondazione IRCCS Ca' Granda Ospedale Maggiore Policlinico · ITHumanitas University · ITUniversity of California, Los Angeles · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Glomerular diseases developing in the kidney allograft are more often recurrences of the original disease affecting the native kidneys. However, in an undefined number of cases de novo, glomerular diseases unrelated to the original disease in the native kidneys can develop in the transplanted kidney. The clinical presentation and histologic features of de novo diseases are often similar to those features observed in patients with primary or secondary GN in the native kidneys. However, in transplanted kidneys, the glomerular, vascular, and tubulointerstitial changes are often intertwined with structural abnormalities already present at the time of transplant or caused by antibody- or cell-mediated allograft rejection, immunosuppressive drugs, or superimposed infection (most often of a viral nature). The pathophysiology of de novo glomerular diseases is quite variable. In rare cases of de novo minimal change disease, circulating factors increasing the glomerular permeability likely participate. Maladaptive hemodynamic changes and tissue fibrosis caused by calcineurin inhibitors or other factors may be involved in the pathogenesis of de novo FSGS. The exposure of cryptic podocyte antigens may favor the development of de novo membranous nephropathy. Many cases of de novo membranoproliferative GN are related to hepatitis C virus infection. Patients with Alport syndrome lacking antigenic epitopes in their glomerular basement membrane may develop antibodies against these glomerular basement membrane antigens expressed in the transplanted kidney. Infection may cause acute GN to have a heterogeneous clinical presentation and outcome. De novo pauci-immune GN in renal transplant is rare. Preexisting or acquired intolerance to glucose may, in the long term, cause diabetic nephropathy. The prognosis of de novo diseases depends on the type of GN, the severity of lesions caused by the alloimmune response, or the efficacy of immunosuppressive therapy. In most cases, the management of de novo glomerular diseases is empirical or elusive.

Indexed as

AnimalsGlomerulonephritisHumansKidney DiseasesKidney GlomerulusKidney TransplantationRisk FactorsTreatment OutcomeGNrenal transplantationtransplant pathology

Identifiers

PMID24700797
PMCPMC4123406
OpenAlexW2171653925

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.