Evidence map›Paper›PMID 19959716›Full record

ArticleJournal of the American Society of Nephrology : JASN2010

A spleen tyrosine kinase inhibitor reduces the severity of established glomerulonephritis.

Jennifer Smith, John P McDaid, Gurjeet Bhangal, Ratana Chawanasuntorapoj, Esteban S Masuda, H Terence Cook, Charles D Pusey, Frederick W K Tam

Open access · greenAbstract read
In one paragraph

Article in Journal of the American Society of Nephrology : JASN, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers.

0numbers the graph read from it
0cells of the map it votes in
31citing papers in PubMed
2.0field-weighted citation impact, top 13% 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

31 citing papers in PubMed, 82 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. Article
  4. Article
  5. Article
  6. Article
  7. Article
  8. Article
  9. Article
  10. Role of spleen tyrosine kinase in liver diseases.World journal of gastroenterology · 2020
    Review
  11. Article
  12. Review
  13. New insights into the pathogenesis of IgA nephropathy.Pediatric nephrology (Berlin, Germany) · 2018
    Review
  14. New and emerging therapies for acute and chronic graftTherapeutic advances in hematology · 2018
    Review
  15. Article
  16. Article
  17. Targeting the tyrosine kinase signalling pathways for treatment of immune-mediated glomerulonephritis: from bench to bedside and beyond.Nephrology, dialysis, transplantation : official publication of the European Dialysis and Transplant Association - European Renal Association · 2017
    Review
  18. Article
  19. Article
  20. Spleen tyrosine kinase contributes to acute renal allograft rejection in the rat.International journal of experimental pathology · 2015
    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

8 authors at 2 institutions in 2 countries.

Jennifer SmithImperial College Kidney and Transplant Institute, Division of Medicine, Hammersmith Hospital, Du Cane Road, London W12 0NN, United Kingdom.
John P McDaid
Gurjeet Bhangal
Ratana Chawanasuntorapoj
Esteban S Masuda
H Terence Cook
Charles D Pusey
Frederick W K Tam
Rigel (United States) · USSiriraj Hospital · TH

Funding

Medical Research Council G0400443
6 · The paper itself

Abstract

Antibody-mediated glomerulonephritis, including that resulting from immune complexes, is an important cause of renal failure and is in need of more specific and effective treatment. Binding of antibody or immune complexes to Fc receptors activates intracellular signal transduction pathways, including spleen tyrosine kinase (Syk), leading to the production of inflammatory cytokines. We examined the effect of R788 (fostamatinib disodium), an oral prodrug of the selective Syk inhibitor R406, in nephrotoxic nephritis in Wistar-Kyoto rats. Treatment with R788 reduced proteinuria, tissue injury, glomerular macrophage and CD8+ cell numbers, and renal monocyte chemoattractant protein-1 (MCP-1) and IL-1beta, even when we started treatment after the onset of glomerulonephritis. When we administered R788 from days 4 to 10, glomerular crescents reduced by 100% (P < 0.01) compared with the vehicle group. When we administered R788 treatment from days 7 to 14, established glomerular crescents reversed (reduced by 21%, P < 0.001), and renal function was better than the vehicle group (P < 0.001). In vitro, R406 downregulated MCP-1 production from mesangial cells and macrophages stimulated with aggregated IgG. These results suggest that Syk is an important therapeutic target for the treatment of glomerulonephritis.

Indexed as

Severity of Illness IndexAminopyridinesAnimalsCells, CulturedChemokine CCL2Disease Models, AnimalGlomerulonephritisInterleukin-1betaIntracellular Signaling Peptides and ProteinsMacrophagesMesangial CellsMorpholinesOxazinesProtein-Tyrosine KinasesPyridinesPyrimidinesAminopyridinesCcl2 protein, ratChemokine CCL2fostamatinibInterleukin-1betaIntracellular Signaling Peptides and ProteinsMorpholinesN4-(2,2-dimethyl-3-oxo-4H-pyrid(1,4)oxazin-6-yl)-5-fluoro-N2-(3,4,5-trimethoxyphenyl)-2,4-pyrimidinediamineOxazinesProtein-Tyrosine KinasesPyridinesPyrimidinesSyk KinaseSyk protein, rat

Identifiers

PMID19959716
PMCPMC2834545
OpenAlexW2129462286

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.