Evidence map›Paper›PMID 33102961›Full record

ArticleKidney international reports2020

Clinical Use of Complement, Inflammation, and Fibrosis Biomarkers in Autoimmune Glomerulonephritis.

Myriam Khalili, Arnaud Bonnefoy, Dominique S Genest, Jérémy Quadri, Jean-Philippe Rioux, Stéphan Troyanov

Open access · goldAbstract read
In one paragraph

Article in Kidney international reports, 2020. 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
2.9field-weighted citation impact, top 8% 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, 32 citations in OpenAlex.

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  12. Identification of inflammatory biomarkers in IgA nephropathy using the NanoString technology: a validation study in Caucasians.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2024
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  18. Alternative pathway diagnostics.Immunological reviews · 2023
    Review
  19. Intertwined pathways of complement activation command the pathogenesis of lupus nephritis.Translational research : the journal of laboratory and clinical medicine · 2022
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  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.

Myriam KhaliliDivision of Nephrology, Hôpital du Sacré-Cœur de Montréal, Quebec, Canada.
Arnaud BonnefoyDivision of Hematology, Centre Hospitalier Universitaire Sainte-Justine, Montréal, Quebec, Canada.
Dominique S GenestDivision of Nephrology, Hôpital du Sacré-Cœur de Montréal, Quebec, Canada.
Jérémy QuadriDivision of Hematology, Centre Hospitalier Universitaire Sainte-Justine, Montréal, Quebec, Canada.
Jean-Philippe RiouxDivision of Nephrology, Hôpital du Sacré-Cœur de Montréal, Quebec, Canada.
Stéphan TroyanovDivision of Nephrology, Hôpital du Sacré-Cœur de Montréal, Quebec, Canada.
Hôpital du Sacré-Cœur de Montréal · CACentre Hospitalier Universitaire Sainte-Justine · CA

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

introductionComplement activation, inflammation, and fibrosis play central roles in the mechanisms of injury in autoimmune glomerulonephritis (GN) but they are seldom assessed in epidemiologic studies. The measurement of urinary biomarkers of these pathways of injury could parallel disease activity and add clinical value beyond proteinuria.

methodsWe performed a prospective cohort study of 100 patients with focal and segmental glomerulosclerosis (FSGS), membranous nephropathy (MN), IgA nephropathy (IgAN), lupus nephritis (LN), anti-neutrophil cytoplasmic autoantibody-associated vasculitis (AAV), and membranoproliferative GN (MPGN) followed for 33 (18-54) months. Repeated urinary samples were collected throughout their follow-up to determine proteinuria, urinary sC5b-9, monocyte chemoattractant protein-1 (MCP-1), and transforming growth factor-beta 1 (TGF-β1), expressed as creatinine ratios. We identified 177 periods of active and inactive disease based on current remission definitions for each disease.

resultsUrinary sC5b-9, MCP-1, and TGF-β1 were present in each disease. In periods leading to a remission, the reduction of urinary sC5b-9 was 91%, greater than for proteinuria with 76%. During inactive periods, those who did not experience a relapse maintained lower levels of biomarkers compared with those who relapsed. At that time, the increase in urinary sC5b-9 was significantly greater than the rise in proteinuria (8.5-fold increase compared with 3.2-fold) and urinary MCP-1 and TGF-β1. Using current remission definitions for each disease, thresholds for each biomarker were determined using receiver operating characteristic curves. Individuals who averaged levels below these cutoffs during their follow-up had better renal outcomes.

conclusionIn autoimmune glomerular diseases, urinary sC5b-9, MCP-1, and TGF-β1 are present and parallel disease activity and outcomes. Urinary sC5b-9 appears to be a more discerning marker of immunologic remissions and relapses.

Indexed as

autoimmune glomerulonephritiscomplementMCP-1sC5b-9TGF-β1urinary biomarkers

Identifiers

PMID33102961
PMCPMC7569694
OpenAlexW3043929167

What OpenQuestion holds

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LicenceCC BY-NC-ND
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.