Evidence map›Paper›PMID 41961272›Full record

ArticlePediatric nephrology (Berlin, Germany)2026

Proteome-wide Mendelian randomization identifies APOM and TNXB as actionable mediators of steroid-sensitive nephrotic syndrome.

Daniel Heydari, Sheldon Langlois, Mahboobeh Norouzi, Robert L Myette, Susan Samuel, Sirui Zhou, Tomoko Takano, Guillaume Butler-Laporte, Mallory L Downie

Abstract read
PubMed Publisher
In one paragraph

Article in Pediatric nephrology (Berlin, Germany), 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing papers in PubMed
–field-weighted citation impact
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

1 citing paper in PubMed.

  1. 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

9 authors.

Daniel HeydariDepartment of Human Genetics, McGill University, Montreal, Canada.
Sheldon LangloisDepartment of Human Genetics, McGill University, Montreal, Canada.
Mahboobeh NorouziResearch Institute of the McGill University Health Centre, Montreal, Canada.
Robert L MyetteChildren's Hospital of Eastern Ontario Research Institute, University of Ottawa, Ottawa, Canada.
Susan SamuelDivision of Pediatric Nephrology, University of British Columbia, Vancouver, Canada.
Sirui ZhouDepartment of Human Genetics, McGill University, Montreal, Canada.
Tomoko TakanoResearch Institute of the McGill University Health Centre, Montreal, Canada.
Guillaume Butler-LaporteDepartment of Human Genetics, McGill University, Montreal, Canada.
Mallory L DownieDepartment of Human Genetics, McGill University, Montreal, Canada. mallory.downie@mcgill.ca.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundDiscovery of autoantibodies in steroid-sensitive nephrotic syndrome (SSNS) has transformed our understanding of SSNS as an immune-mediated disease; however, mechanisms underlying autoantibody production are unknown. Current treatments for SSNS are non-targeted and cause serious adverse effects. We sought to identify circulating proteins with a causal relationship to SSNS, which likely reflect underlying immune derangements, using an unbiased two-sample Mendelian randomization (MR) and colocalization approach to inform novel drug targets for disease.

methodsSummary-level data from eight large independent proteome-wide association studies were used to estimate the causal effect of 1540 proteins on SSNS risk by Mendelian randomization (MR) using cis genetic determinants (protein quantitative trait loci, pQTL). Genetic colocalization, gene expression, and affinity binding analyses were performed to further investigate loci identified by MR.

resultsTwo proteins, apolipoprotein M (APOM) and Tenascin XB (TNXB), were causally linked to SSNS by MR and colocalization analysis. Increases in APOM and TNXB levels were associated with decreased risk of SSNS (p = 1.37 × 10

conclusionsWe identified APOM and TNXB as novel blood proteins associated with SSNS in children. These proteins are promising targets for the development or repurposing of drugs as novel treatments for SSNS.

Indexed as

Apolipoproteins MNephrotic SyndromeTenascinAutoantibodiesGenome-Wide Association StudyHLA-DQ alpha-ChainsHumansMendelian Randomization AnalysisProteomeQuantitative Trait LociSteroidsApolipoproteins MAutoantibodiesHLA-DQA1 antigenHLA-DQ alpha-ChainsProteomeSteroidsTenascintenascin XAPOMColocalizationGWASHLAMendelian randomizationNephrologyPediatricsProteomicsSteroid-sensitive nephrotic syndromeTNXB

Identifiers

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.