Evidence map›Paper›PMID 26423803›Full record

ArticleJournal of nephrology2016

Epidermal growth factor receptor inhibition with erlotinib ameliorates anti-Thy 1.1-induced experimental glomerulonephritis.

Jukka M Rintala, Johanna Savikko, Sini E Rintala, Niina Palin, Petri K Koskinen

Abstract read
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In one paragraph

Article in Journal of nephrology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.

0numbers the graph read from it
0cells of the map it votes in
6citing papers in PubMed
0.7field-weighted citation impact, top 26% 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

6 citing papers in PubMed, 13 citations in OpenAlex.

  1. Review
  2. Article
  3. Article
  4. iRhom2 promotes lupus nephritis through TNF-α and EGFR signaling.The Journal of clinical investigation · 2018
    Article
  5. 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
  6. 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

5 authors at 2 institutions in 1 country.

Jukka M RintalaTransplantation Laboratory, University of Helsinki, P.O. Box 21, Haartmaninkatu 3, 00014, Helsinki, Finland. jukka.m.rintala@helsinki.fi.
Johanna SavikkoTransplantation Laboratory, University of Helsinki, P.O. Box 21, Haartmaninkatu 3, 00014, Helsinki, Finland.
Sini E RintalaTransplantation Laboratory, University of Helsinki, P.O. Box 21, Haartmaninkatu 3, 00014, Helsinki, Finland.
Niina PalinTransplantation Laboratory, University of Helsinki, P.O. Box 21, Haartmaninkatu 3, 00014, Helsinki, Finland.
Petri K KoskinenTransplantation Laboratory, University of Helsinki, P.O. Box 21, Haartmaninkatu 3, 00014, Helsinki, Finland.
University of Helsinki · FIHelsinki University Hospital · FI

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundMesangial proliferative glomerulonephritis is a common glomerular disorder that may lead to end-stage renal disease. Epidermal growth factor (EGF) plays an important role in the regulation of cell growth, proliferation, and differentiation and in the pathology of various renal diseases. Erlotinib is a novel, oral, highly selective tyrosine kinase inhibitor of the EGF receptor. It is clinically used to treat non-small cell lung and pancreatic cancers. Here, we investigated the effect of erlotinib on the progression of mesangioproliferative glomerulonephritis in an experimental model.

methodsMesangial glomerulonephritis was induced with anti-rat Thy-1.1 antibody in male Wistar rats weighing 150-160 g. Rats were treated with erlotinib (10 mg/kg/day p.o.) or vehicle only (polyethylene glycol). Native Wistar rat kidneys were used as histological controls. Serum creatinine levels were measured at day 7. Kidneys were harvested 7 days after antibody administration for histology.

resultsNative controls showed no histological signs of glomerular pathology. In the vehicle group, intense glomerular inflammation developed after 7 days and prominent mesangial cell proliferation and glomerular matrix accumulation was seen. Erlotinib was well tolerated and there were no adverse effects during the follow-up period. Erlotinib significantly prevented progression of the glomerular inflammatory response and glomerular mesangial cell proliferation as well as matrix accumulation when compared with the vehicle group. Erlotinib also preserved renal function.

conclusionThese results indicate that erlotinib prevents the early events of experimental mesangial proliferative glomerulonephritis. Therefore, inhibition of the EGF receptor with erlotinib could prevent the progression of glomerulonephritis also in clinical nephrology.

Indexed as

AnimalsCreatinineErbB ReceptorsErlotinib HydrochlorideGlomerulonephritisIsoantibodiesKidneyMaleRatsRats, Wistaranti-Thy antibodyCreatinineErbB ReceptorsErlotinib HydrochlorideIsoantibodiesEpidermal growth factorErlotinibExperimental glomerulonephritis

Identifiers

PMID26423803
OpenAlexW2198564483

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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.