ArticlePediatric nephrology (Berlin, Germany)2026
Proteome-wide Mendelian randomization identifies APOM and TNXB as actionable mediators of steroid-sensitive nephrotic syndrome.
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.
What it found
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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.
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Who cites it
1 citing paper in PubMed.
- APOM-S1P axis as a therapeutic target in steroid sensitive nephrotic syndrome.Pediatric nephrology (Berlin, Germany) · 2026Article
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Authors and funding
9 authors.
Funding
No grant is acknowledged in the PubMed record.
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.
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