ArticleClinical kidney journal2026
Protocadherin FAT1-associated membranous nephropathy after hematopoietic stem cell transplantation-a cohort study with clinico-pathological correlations.
Article in Clinical kidney journal, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 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
2 citing papers in PubMed.
- FAT1-associated membranous nephropathy after hematopoietic stem cell transplantation: a case report and review of the literature.CEN case reports · 2026Review
- Model-Informed Precision Dosing of Tacrolimus Initial Dosage Optimization in Membranous Nephropathy Patients.Drug design, development and therapy · 2026Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
8 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Background: The identification of causative antigens for membranous nephropathy (MN) has revolutionized the comprehension of the pathophysiology of this autoimmune disease and its management. Recently, some studies described protocadherin FAT1 (FAT1) as a causal antigen in the context of hematopoietic stem cell transplantation (HSCT). The aim of this study was to investigate the large Viennese kidney biopsy collection at the Department of Pathology of the Medical University of Vienna and explore MN cases after HSCT for the causative antigen. Methods: Fifteen patients were identified with MN in diagnostic renal biopsies for proteinuria/nephrotic syndrome after HSCT between 2001 and 2024. Cases were reviewed and tested for the expression of FAT1 by immunofluorescence specifically. Results: Immunofluorescence showed that 12 out of 15 patients with MN had FAT1 expression, appearing 2.3 years after HSCT. In three patients without FAT1 expression, MN appeared 3.8 years after HSCT, with one testing positive for phospholipase A2 receptor (PLA2R) and two with unknown antigens. Serum creatinine for FAT1+ MN was 1.2 mg/dl, while FAT1- MN was 1.3 mg/dl. Proteinuria was 8 g/g compared to 10.4 g/g, respectively. IgG4 positivity was seen in 30% of FAT1+ MN cases. Over a follow up of 5.2 years, of the seven FAT1+ MN patients treated with rituximab, four achieved complete remission, two partial remission, and one was non-responsive. Conclusion: This hitherto largest single-center-cohort solidifies FAT1 as a causative antigen for MN in the setting of HSCT. However, not all post-HSCT-MN are related to FAT1.
Indexed as
Identifiers
What OpenQuestion holds
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.