ArticleBMC nephrology2022
Proteomic signature of tubulointerstitial tissue predicts prognosis in IgAN.
Article in BMC nephrology, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers, 1 of them a synthesis that pooled it.
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Who cites it
8 citing papers in PubMed, 1 synthesis or guideline pooled it, 8 citations in OpenAlex.
- The current use of proteomics and metabolomics in glomerulonephritis: a systematic literature review.Journal of nephrology · 2024Pooled it
- Plasma Proteomics in IgA Nephropathy: From Circulating Biomarkers to Molecular Endotypes.Cells · 2026Review
- External validation of a nomogram for predicting tubulointerstitial lesions in IgA nephropathy: a cross-regional study in China.Clinics (Sao Paulo, Brazil) · 2026Article
- Serum proteome analysis detects early molecular signatures of disease progression in IgA nephropathy.Clinical kidney journal · 2025Article
- Spatial proteomics to discover aging-associated alterations in the renal tubulointerstitium.Clinical proteomics · 2025Article
- ADAMTS13 attenuates renal fibrosis by suppressing thrombospondin 1 mediated TGF-β1/Smad3 activation.Toxicology and applied pharmacology · 2025Article
- Kidney Disease and Proteomics: A Recent Overview of a Useful Tool for Improving Early Diagnosis.Advances in experimental medicine and biology · 2024Article
- Identification and validation of glomerulotubular crosstalk genes mediating IgA nephropathy by integrated bioinformatics.BMC nephrology · 2022Article
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundIgA nephropathy (IgAN) is associated with a significant risk of progression to kidney failure. Tubular atrophy is an established important risk factor for progressive disease, but few studies have investigated tubulointerstitial molecular markers and mechanisms of progression in IgAN.
methodsBased on data from the Norwegian Renal Registry, two groups were included: IgAN patients with (n = 9) or without (n = 18) progression to kidney failure during 10 years of follow-up. Tubulointerstitial tissue without discernible interstitial expansion or pronounced tubular alterations was microdissected, proteome was analysed using tandem mass spectrometry and relative protein abundances were compared between groups.
resultsProteome analyses quantified 2562 proteins with at least 2 unique peptides. Of these, 150 proteins had significantly different abundance between progressive and non-progressive IgAN patients, 67 were more abundant and 83 less abundant. Periostin was the protein with the highest fold change between progressive and non-progressive IgAN (fold change 8.75, p < 0.05) and periostin staining was also stronger in patients with progressive vs non-progressive IgAN. Reactome pathway analyses showed that proteins related to inflammation were more abundant and proteins involved in mitochondrial translation were significantly less abundant in progressive vs non-progressive patients.
conclusionsMicrodissection of tubulointerstitial tissue with only mild damage allowed for identification of proteome markers of early progressive IgAN. Periostin abundance showed promise as a novel and important risk marker of progression.
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