Evidence map›Paper›PMID 25715120›Full record

ArticleKidney international2015

Correlation of disease activity in proliferative glomerulonephritis with glomerular spleen tyrosine kinase expression.

Stephen P McAdoo, Gurjeet Bhangal, Theresa Page, H Terence Cook, Charles D Pusey, Frederick W K Tam

Open access · greenAbstract read
In one paragraph

Article in Kidney international, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.

0numbers the graph read from it
0cells of the map it votes in
28citing papers in PubMed
1.8field-weighted citation impact, top 15% 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

28 citing papers in PubMed, 46 citations in OpenAlex.

  1. The Src-Family Kinases Hck, Fgr and Lyn Drive Immune Complex-Mediated Glomerulonephritis Through the Syk Tyrosine Kinase.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2026
    Article
  2. Review
  3. Review
  4. Review
  5. Article
  6. IgA nephropathy.Nature reviews. Disease primers · 2023
    Review
  7. Article
  8. Article
  9. Review
  10. Article
  11. Article
  12. Review
  13. Article
  14. New therapeutic perspectives for IgA nephropathy in children.Pediatric nephrology (Berlin, Germany) · 2021
    Review
  15. Review
  16. Emerging Modes of Treatment of IgA Nephropathy.International journal of molecular sciences · 2020
    Review
  17. Article
  18. Article
  19. New strategies and perspectives on managing IgA nephropathy.Clinical and experimental nephrology · 2019
    Review
  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

6 authors at 2 institutions in 1 country.

Stephen P McAdooRenal and Vascular Inflammation Section, Department of Medicine, Imperial College London, Hammersmith Hospital, London, UK.
Gurjeet BhangalRenal and Vascular Inflammation Section, Department of Medicine, Imperial College London, Hammersmith Hospital, London, UK.
Theresa PageRenal and Vascular Inflammation Section, Department of Medicine, Imperial College London, Hammersmith Hospital, London, UK.
H Terence CookCentre for Complement and Inflammation Research, Imperial College London London, UK.
Charles D PuseyRenal and Vascular Inflammation Section, Department of Medicine, Imperial College London, Hammersmith Hospital, London, UK.
Frederick W K TamRenal and Vascular Inflammation Section, Department of Medicine, Imperial College London, Hammersmith Hospital, London, UK.
Hammersmith Hospital · GBCentre for Inflammation Research · GB

Funding

Medical Research Council G0400443Medical Research Council G0901997Medical Research Council G0901997/1
6 · The paper itself

Abstract

Spleen tyrosine kinase (SYK) is an important component of the intracellular signaling pathway for various immunoreceptors. Inhibition of SYK has shown promise in preclinical models of autoimmune and glomerular disease. However, the description of SYK expression in human renal tissue, which would be desirable ahead of clinical studies, is lacking. Here we conducted immunohistochemical analysis for total and phosphorylated SYK in biopsy specimens from >120 patients with a spectrum of renal pathologies, including thin basement membrane lesion, minimal change disease, membranous nephropathy, IgA nephropathy, lupus nephritis, ANCA-associated glomerulonephritis, antiglomerular basement membrane disease, and acute tubular necrosis. We found significant SYK expression in proliferative glomerulonephritis and that glomerular expression levels correlated with presenting serum creatinine and histological features of disease activity that predict outcome in IgA nephropathy, lupus nephritis, ANCA-associated glomerulonephritis, and antiglomerular basement membrane disease. SYK was phosphorylated within pathological lesions, such as areas of extracapillary and endocapillary proliferation, and appeared to localize to both infiltrating leucocytes and to resident renal cells within diseased glomeruli. Thus SYK is associated with the pathogenesis of proliferative glomerulonephritides, suggesting that these conditions may respond to SYK inhibitor treatment.

Indexed as

Antigens, CDAntigens, Differentiation, MyelomonocyticCapillariesCD68 MoleculeCreatinineEpithelial CellsGlomerulonephritisHumansIntracellular Signaling Peptides and ProteinsKidney GlomerulusKidney Tubules, DistalLeukocytesNeovascularization, PathologicPhosphorylationProtein-Tyrosine KinasesSyk KinaseAntigens, CDAntigens, Differentiation, MyelomonocyticCD68 antigen, humanCD68 MoleculeCreatinineIntracellular Signaling Peptides and ProteinsProtein-Tyrosine KinasesSyk KinaseSYK protein, human

Identifiers

PMID25715120
PMCPMC4488852
OpenAlexW2015552327

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Registered trials

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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.