Evidence map›Paper›PMID 35369552›Full record

ReviewKidney3602020

Fibrillary Glomerulonephritis and DnaJ Homolog Subfamily B Member 9 (DNAJB9).

Nattawat Klomjit, Mariam Priya Alexander, Ladan Zand

Open access · diamondAbstract readReview
In one paragraph

Review in Kidney360, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.

0numbers the graph read from it
0cells of the map it votes in
19citing papers in PubMed
1.0field-weighted citation impact, top 25% 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

19 citing papers in PubMed, 27 citations in OpenAlex.

  1. Article
  2. Atypical Anti-Glomerular Basement Membrane Disease.Kidney international reports · 2026
    Article
  3. Article
  4. Targeting CD20 for B-cell Depletion in Autoimmune Kidney Disease: Next Generation.BioDrugs : clinical immunotherapeutics, biopharmaceuticals and gene therapy · 2025
    Review
  5. Article
  6. Article
  7. Article
  8. Article
  9. Fibrillary Glomerulonephritis Diagnosis Is Enhanced by DNAJB9: Three Cases with Different Clinical, Anatomopathologic Features and Outcomes.Pathophysiology : the official journal of the International Society for Pathophysiology · 2025
    Article
  10. Article
  11. Article
  12. Article
  13. Article
  14. Article
  15. Article
  16. Review
  17. Review
  18. Article
  19. 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

3 authors at 2 institutions in 1 country.

Nattawat KlomjitDivision of Nephrology and Hypertension, Mayo Clinic, Rochester, Minnesota.
Mariam Priya AlexanderDivision of Nephrology and Hypertension, Mayo Clinic, Rochester, Minnesota.
Ladan ZandDivision of Nephrology and Hypertension, University of Minnesota, Minneapolis, Minnesota.
Mayo Clinic · USUniversity of Minnesota · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Fibrillary GN (FGN) is a rare glomerular disease that is diagnosed based on the presence of fibrils in glomeruli. The fibrils are typically noncongophilic, randomly oriented, and measure 12-24 nm. Traditionally, electron microscopy (EM) has been an important tool to aid in the diagnosis of FGN by identifying the fibrils and to distinguish it from other entities that could mimic FGN. However, recently DnaJ homolog subfamily B member 9 (DNAJB9) has emerged as both a specific and sensitive biomarker in patients with FGN. It allows prompt diagnosis and alleviates reliance on EM. DNAJB9 is a cochaperone of heat shock protein 70 and is involved in endoplasmic reticulum protein-folding pathways. But its role in the pathogenesis of FGN remains elusive. DNAJB9 may act as a putative antigen or alternatively it may secondarily bind to misfolded IgG in the glomeruli. These hypotheses need future studies to elucidate the role of DNAJB9 in the pathogenesis of FGN. The treatment regimen for FGN has been limited due to paucity of studies. Most patients receive combination immunosuppressive regimens. Rituximab has been studied the most in FGN and it may delay disease progression. Prognosis of FGN remains poor and 50% require dialysis within 2 years of diagnosis. Despite its poor prognosis in native kidneys, the rate of recurrence post-transplantation is low (20%) and patient as well as allograft outcomes are similar to patients without FGN.

Indexed as

GlomerulonephritisHSP40 Heat-Shock ProteinsHumansMembrane ProteinsMolecular ChaperonesRenal DialysisDNAJB9 protein, humanHSP40 Heat-Shock ProteinsMembrane ProteinsMolecular ChaperonesDNAJB9fibrillary glomerulonephritisglomerular and tubulointerstitial diseaseskidney glomerulusproteinuriarituximab

Identifiers

PMID35369552
PMCPMC8815599
OpenAlexW3040887644

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.