ArticleKidney3602021
Transforming Growth Factor Beta Receptor 3 (TGFBR3)-Associated Membranous Nephropathy.
Article in Kidney360, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers.
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.
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.
Who cites it
31 citing papers in PubMed, 57 citations in OpenAlex.
- Human biomarker navigator.iMeta · 2026Review
- Integrative gene target mapping, RNA sequencing, in silico molecular docking, ADMET profiling and molecular dynamics simulation study of marine derived molecules for type 1 diabetes mellitus.Molecular diversity · 2026Article
- Proteomic Profiling of Complement Components in Glomerular Disease.Laboratory investigation; a journal of technical methods and pathology · 2026Article
- Membranous Nephropathy: Antigenic Landscape and a Novel Pathogenetic Model.International journal of molecular sciences · 2026Review
- Contemporary review of primary membranous nephropathy.Frontiers in immunology · 2026Review
- Extracellular Vesicular Proteins in Plasma from Patients with Cutaneous Lupus Correlate with Disease Activity.Current issues in molecular biology · 2025Article
- Antigens in membranous nephropathy: discovery and clinical implications.Nature reviews. Nephrology · 2025Review
- The importance of identifying new and putative target antigens associated with membranous nephropathy: evidence from a Sardinian cohort.Clinical kidney journal · 2025Article
- Questions and Caveats in Antigen-Defined Membranous Nephropathy.Journal of the American Society of Nephrology : JASN · 2025Review
- Article
- Membranous nephropathy - an antigen-specific disease: a paradigm shift in the understanding of this disease.International journal of clinical and experimental pathology · 2025Article
- Antibodies Against Anti-Oxidant Enzymes in Autoimmune Glomerulonephritis and in Antibody-Mediated Graft Rejection.Antioxidants (Basel, Switzerland) · 2024Article
- Technology Innovation for Discovering Renal Autoantibodies in Autoimmune Conditions.International journal of molecular sciences · 2024Review
- Review
- Membranous nephropathy: pathogenesis and treatments.MedComm · 2024Review
- Glomerular Exostosin-Positivity is Associated With Disease Activity and Outcomes in Patients With Membranous Lupus Nephritis.Kidney international reports · 2024Article
- NELL1 membranous nephropathy: clinical associations provide mechanistic clues.Frontiers in nephrology · 2024Review
- How to Choose the Right Treatment for Membranous Nephropathy.Medicina (Kaunas, Lithuania) · 2023Review
- Clinical and Histopathologic Characteristics of Pediatric Patients With Primary Membranous Nephropathy.Kidney international reports · 2023Article
- Future landscape for the management of membranous nephropathy.Clinical kidney journal · 2023Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
10 authors at 3 institutions in 1 country.
Funding
Abstract
Background: Membranous lupus nephritis (MLN) comprises 10%-15% of lupus nephritis and increases morbidity and mortality of patients with SLE through complications of nephrotic syndrome and chronic kidney failure. Identification of the target antigens in MLN may enable noninvasive monitoring of disease activity, inform treatment decisions, and aid in prognostication, as is now possible for idiopathic MN caused by antibodies against the phospholipase A2 receptor. Here, we show evidence for type III TGF- Methods: Mass spectrometry was used for protein discovery through enrichment of glomerular proteins by laser capture microdissection and through elution of immune complexes within MLN biopsy specimens. Colocalization with IgG within glomerular immune deposits from patients and disease controls was evaluated by confocal microscopy. Immunostaining of consecutive case series was used to determine the overall frequency in MN and MLN. Results: TGFBR3 was found to be enriched in glomeruli and coimmunoprecipitated with IgG within a subset of MLN biopsy specimens by mass spectrometry. Staining of consecutive MN cases without clinical evidence of SLE did not show TGFBR3 expression (zero of 104), but showed a 6% prevalence in MLN (11 of 199 cases). TGFBR3 colocalized with IgG along the glomerular basement membranes in TGFBR3-associated MN, but not in controls. Conclusions: Positive staining for TGFBR3 within glomerular immune deposits represents a distinct form of MN, substantially enriched in MLN. A diagnosis of TGFBR3-associated MN can alert the clinician to search for an underlying autoimmune disease.
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Registered trials
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.