ArticleKidney medicine2026
Anti-Contactin-1-Associated Membranous Nephropathy Presenting With Subsequent Autoimmune Nodopathy.
Article in Kidney medicine, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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
0 citing papers in PubMed.
No citing paper in PubMed yet.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
7 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
A 70-year-old man presented with biopsy-proven phospholipase A2 receptor--negative membranous nephropathy (MN). Shortly thereafter, he presented with progressive sensorimotor polyneuropathy, initially consistent with an inflammatory demyelinating polyneuropathy. Laboratory testing revealed strongly positive anti-contactin-1 (CNTN1) autoantibodies, a rare antigen target recently implicated in a subset of MN patients with concurrent inflammatory demyelinating polyneuropathy, reclassifying it as an autoimmune nodopathy. Intensive immunosuppressive treatment including methylprednisolone, cyclophosphamide, plasmapheresis, intravenous immunoglobulins, and rituximab led to significant neurological improvement and seronegativity for anti-CNTN1 antibodies. Nephrotic syndrome improved gradually with partial remission observed 2 years after treatment initiation. This case highlights the autoimmune overlap of MN and autoimmune nodopathy mediated by anti-CNTN1 antibodies, targeting shared epitopes in podocytes and the paranodal region of myelinated peripheral nerves. It underscores the clinical importance of screening for novel antibodies in phospholipase A2 receptor--negative MN patients, particularly anti-CNTN1 when neurological symptoms develop. This report supports aggressive immunosuppression tailored to antibody-mediated disease and suggests anti-CNTN1 titers as a biomarker for monitoring therapeutic response.
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.