ArticleKidney international reports2025
Persistent Chronic Thrombo-Inflammation in Anti-Glomerular Basement Membrane Disease Despite Immune Complex Removal.
Article in Kidney international reports, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
Introduction: Anti-glomerular basement membrane (anti-GBM) disease is a severe autoimmune disease characterized by autoantibody-mediated glomerular damage, leading to a rapid decline in kidney function and end-stage renal disease. The stimulation of megakaryopoiesis (Mkpoiesis) and platelet production, driven by kidney-derived hematopoietic growth factors (HGFs) such as thrombopoietin (TPO), exacerbates chronic thrombosis and inflammation. Activated platelets release bioactive molecules able to promote microvascular dysfunction, cell proliferation, and excessive extracellular matrix deposition in injured glomeruli. Understanding the molecular mechanisms driving persistent thrombo-inflammation during anti-GBM disease will enhance therapeutic improvements. The hypothesis of this study was that anti-GBM disease could stimulate the production of kidney-derived HGFs and proinflammatory mediators. In addition, immobilized anti-GBM antibodies in glomeruli could directly activate FcγRIIA expressing platelets, thereby promoting chronic platelet activation during anti-GBM disease. Methods: In the GOOD-IDES-01 trial, patients received, in addition to standard care, imlifidase (the IgG-degrading enzyme, IdeS). In plasma samples collected from patients with anti-GBM disease, before and after imlifidase treatment, and from healthy blood donors (HBDs), we analyzed plasma HGFs, proinflammatory and platelet activation markers, and platelet-derived products. Results: Anti-GBM disease significantly elevated plasma proinflammatory and platelet activation markers, and HGFs (TPO and stem cell factor [SCF]). Plasma TPO correlated with anti-GBM titers. Standard care and imlifidase treatment only reduced TPO levels and platelet counts. Platelet activation markers (CD62P and Tlt1) strongly correlated with platelet-derived products (PDGF, CCL5, PF4, and TGFβ) during the active phase of the disease, but remained elevated despite the treatment. Conclusion: Circulating HGFs, proinflammatory cytokines, and platelet activation markers are important biomarkers of anti-GBM disease activity. Chronic platelet activation, persists independently of anti-GBM antibody integrity, highlighting the need for therapies targeting thrombo-inflammation.
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