ArticlePediatric nephrology (Berlin, Germany)2012
TNFα pathway blockade ameliorates toxic effects of FSGS plasma on podocyte cytoskeleton and β3 integrin activation.
Article in Pediatric nephrology (Berlin, Germany), 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 39 papers.
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Who cites it
39 citing papers in PubMed, 59 citations in OpenAlex.
- Intrinsic tumor necrosis factor-α pathway is activated in a subset of patients with focal segmental glomerulosclerosis.PloS one · 2019Trial
- Immune podocyte injury in autoimmune glomerular diseases.Frontiers in immunology · 2026Review
- Vincristine Treatment Protects Against Podocyte Damage in Focal Segmental Glomerulosclerosis.Kidney international reports · 2025Article
- Emerging roles of non-coding RNAs in idiopathic nephrotic syndrome: a narrative review.BMC nephrology · 2025Review
- Past and future in vitro and in vivo approaches toward circulating factors and biomarkers in idiopathic nephrotic syndrome.Pediatric nephrology (Berlin, Germany) · 2025Review
- Personalized disease recurrence modeling using iPSC-derived podocytes in patients with idiopathic nephrotic syndrome.Nephrology, dialysis, transplantation : official publication of the European Dialysis and Transplant Association - European Renal Association · 2025Article
- Engineered 3D Kidney Glomerular Microtissues to Model Podocyte-Centric Diseases for the Validation of New Drug Targets.Advanced healthcare materials · 2025Article
- MicroRNAs in idiopathic childhood nephrotic syndrome.Clinical and experimental nephrology · 2025Article
- Article
- Swollen Feet: Considering the Paradoxical Roles of Interleukins in Nephrotic Syndrome.Biomedicines · 2024Review
- suPAR and WT1 modify the adhesion of podocytes and are related to proteinuria in class IV lupus nephritis.Journal of translational autoimmunity · 2023Article
- What is circulating factor disease and how is it currently explained?Pediatric nephrology (Berlin, Germany) · 2023Review
- Preliminary study of anti-CD40 and ubiquitin proteasome antibodies in primary podocytopaties.Frontiers in medicine · 2023Article
- Ion channels and channelopathies in glomeruli.Physiological reviews · 2023Review
- Trends in pediatric nephrotic syndrome.World journal of nephrology · 2021Review
- Nephrotic syndrome in a dish: recent developments in modeling in vitro.Pediatric nephrology (Berlin, Germany) · 2020Review
- Role of A20/TNFAIP3 deficiency in lupus nephritis in MRL/lpr mice.Clinical and experimental nephrology · 2020Article
- Autoimmunity in Focal Segmental Glomerulosclerosis: A Long-Standing Yet Elusive Association.Frontiers in medicine · 2020Review
- Wenyang Lishui Decoction Ameliorates Podocyte Injury in Membranous Nephropathy Rat and Cell Models by Regulating p53 and Bcl-2.Evidence-based complementary and alternative medicine : eCAM · 2020Article
- Molecular stratification of idiopathic nephrotic syndrome.Nature reviews. Nephrology · 2019Review
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Authors and funding
5 authors at 3 institutions in 2 countries.
Funding
Abstract
backgroundIn the absence of mutant genes encoding components of the podocyte slit diaphragm, about 30-50 % of children with primary glucocorticoid-resistant focal segmental glomerulosclerosis (FSGS) develop recurrent proteinuria and slowly progressive FSGS lesions following renal transplantation. Recurrence of FSGS in the allograft strongly suggests a circulating factor that disturbs normal podocyte biology. To date, the nature of the circulating factor is unclear, and there is no cure for the recurrent form of FSGS (R-FSGS).
methodsCultured differentiated human podocytes were exposed to the plasmapheresis effluent or blood plasma samples from pediatric patients with recurrent or primary FSGS; in some cases, podocytes were pre-incubated with specific antibodies to block the tumor necrosis factor-alpha (TNFα) signaling pathway. Integrity of focal adhesion complexes and actin cytoskeleton were investigated by immunofluorescent microscopy.
resultsPlasmapheresis effluent from an R-FSGS child or fresh plasma from two children with primary FSGS rapidly disturbed the cytoskeleton of normal human podocytes in vitro. Plasma from a child with R-FSGS also activated β3 integrin and dispersed focal adhesion complexes. The effects were reversed by pre-incubation with antibodies against TNFα or either of the two TNFα receptors. When our patient with R-FSGS became resistant to plasmapheresis, we initiated treatment with twice weekly etanercept injections and then infliximab. Within 3 weeks of regular anti-TNFα therapy, the patient achieved sustained partial remission of proteinuria, allowing us to wean her off plasmapheresis completely.
conclusionsWe suggest that in some FSGS patients, disruption of the podocyte cytoskeleton and β3 integrin-mediated podocyte attachment are driven by the TNFα pathway.
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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.