Evidence map›Paper›PMID 30451735›Full record

ReviewCurrent opinion in nephrology and hypertension2019

Unmet challenges in membranous nephropathy.

David J Salant

Abstract readReview
In one paragraph

Review in Current opinion in nephrology and hypertension, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
21citing papers in PubMed, 1 pooled it
3.5field-weighted citation impact, top 7% 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

21 citing papers in PubMed, 1 synthesis or guideline pooled it, 34 citations in OpenAlex.

  1. Pooled it
  2. Trial
  3. Trial
  4. Trial
  5. Review
  6. Article
  7. Review
  8. Review
  9. Review
  10. Review
  11. Review
  12. Review
  13. Lupus Membranous Nephropathy.Glomerular diseases · 2021
    Review
  14. Article
  15. Article
  16. Chylomicronemia from GPIHBP1 autoantibodies.Journal of lipid research · 2020
    Review
  17. Review
  18. Advances in Pathogenesis of Idiopathic Membranous Nephropathy.Kidney diseases (Basel, Switzerland) · 2020
    Review
  19. Article
  20. 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

1 author at 1 institution in 1 country.

David J SalantDepartment of Medicine, Boston University School of Medicine and Section of Nephrology, Boston Medical Center, Boston, Massachusetts, USA.
Boston University · US

Funding

RESEARCH TRAINING IN NEPHROLOGYT32DK007053 · NIDDK · BOSTON UNIVERSITY MEDICAL CAMPUS · PI RIFKIN, IAN R · 1986 to 2019
$3.9M
NIDDK NIH HHS T32 DK007053
6 · The paper itself

Abstract

purpose of reviewDespite major advances in since the discovery of the phospholipase A2 receptor (PLA2R) as the major autoantigen on podocytes in primary membranous nephropathy, there are still several unanswered questions as highlighted here. RECENT

findingsA substantial body of literature, included in more than 680 articles since 2009, has documented genetic susceptibility to primary membranous nephropathy involving PLA2R1 and class II MHC alleles, the clinical value of anti-PLA2R assays, the significance of epitope spreading of the anti-PLA2R response, discovery of thrombospondin type I domain-containing 7A (THSD7A) as a minor antigen in primary membranous nephropathy, and the ability to transfer disease into mice by infusion of anti-THSD7A sera. However, the normal physiology and pathophysiology of PLA2R and THSD7A in podocytes is still unknown and the genetic influence on disease susceptibility is unexplained. We still do not know what causes loss of self-tolerance to PLA2R and THSD7A or how the autoantibodies, which are predominantly of the IgG4 subclass, cause podocyte injury and proteinuria. Complement deposits are prominent in membranous nephropathy but we are still uncertain how the complement system is activated and whether or not it plays a role in podocyte damage. Notwithstanding the advances over the past decade, our treatments have not changed substantially. SUMMARY: This review identifies opportunities to extend the advances that have been made to better understand the immunopathogenesis and genetic basis of primary membranous nephropathy and apply the knowledge to design more specific therapies.

Indexed as

AutoantibodiesComplement System ProteinsGenes, MHC Class IIGlomerulonephritis, MembranousHumansPodocytesProteinuriaReceptors, Phospholipase A2ThrombospondinsAutoantibodiesComplement System ProteinsReceptors, Phospholipase A2ThrombospondinsTHSD7A protein, human

Identifiers

PMID30451735
PMCPMC6289589
OpenAlexW2901167638

What OpenQuestion holds

Textmetadata
LicenceTDM
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.