{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,6,1]],"date-time":"2026-06-01T10:07:52Z","timestamp":1780308472805,"version":"3.54.0"},"reference-count":48,"publisher":"Oxford University Press (OUP)","license":[{"start":{"date-parts":[[2026,5,13]],"date-time":"2026-05-13T00:00:00Z","timestamp":1778630400000},"content-version":"am","delay-in-days":0,"URL":"https:\/\/academic.oup.com\/journals\/pages\/open_access\/funder_policies\/chorus\/standard_publication_model"}],"funder":[{"DOI":"10.13039\/501100001809","name":"National Natural Science Foundation of China","doi-asserted-by":"publisher","award":["82325009"],"award-info":[{"award-number":["82325009"]}],"id":[{"id":"10.13039\/501100001809","id-type":"DOI","asserted-by":"publisher"}]},{"name":"National High Level Hospital Clinical Research Funding","award":["2023HQ07"],"award-info":[{"award-number":["2023HQ07"]}]}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":[],"abstract":"<jats:title>ABSTRACT<\/jats:title>\n                  <jats:sec>\n                    <jats:title>Background and hypothesis<\/jats:title>\n                    <jats:p>Thromboembolism is a serious complication of nephrotic syndrome and occurs disproportionately in membranous nephropathy (MN). Whether anti-phospholipase A2 receptor (PLA2R) antibodies and complement activation directly promote endothelial dysfunction and thrombosis is unclear.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Methods<\/jats:title>\n                    <jats:p>In a retrospective cohort of biopsy-proven MN (n = 45 with thromboembolism; 1:2 time-selected controls), we quantified anti-PLA2R antibodies, C3a, and C5a and analyzed their associations with thromboembolic events. Using human umbilical vein endothelial cells (HUVECs), we tested MN plasma, purified anti-PLA2R IgG (including IgG4), and IgG fragments, and interrogated Fc and complement receptor pathways. Readouts included pro\/anticoagulant factor expression, inflammasome\/pyroptosis activation, and secreted mediators.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Results<\/jats:title>\n                    <jats:p>Anti-PLA2R levels were higher in patients with thromboembolism than in those without and correlated with D-dimer and fibrin degradation products. A ROC-derived threshold of 92 RU\/ml was associated with greater thromboembolic risk. MN plasma and anti-PLA2R IgG induced a dose- and time-dependent procoagulant phenotype in HUVECs, upregulating tissue factor (TF), ICAM-1, and PAI-1 and increasing supernatant TF and sICAM-1. The Fc fragment reproduced these effects, whereas F(ab\u2019)2 did not. Anti-PLA2R colocalized with Fc\u03b3RI; Fc\u03b3RI silencing abrogated procoagulant responses and reduced NLRP3, caspase-1 p20, GSDMD-N, IL-1\u03b2, and IL-18. The NLRP3 inhibitor similarly suppressed pyroptosis and procoagulant readouts. Complement anaphylatoxins C3a\/C5a further increased TF\/ICAM-1 via C3aR\/C5aR, and antagonists reversed MN-plasma\u2013induced effects.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Conclusions<\/jats:title>\n                    <jats:p>Anti-PLA2R antibodies promote endothelial pyroptosis and a TF-high procoagulant phenotype through Fc\u03b3RI signaling in vitro.<\/jats:p>\n                    <jats:p>Complement signaling amplifies this response. Targeting Fc\u03b3RI-inflammasome pathways may mitigate thromboembolic risk in MN.<\/jats:p>\n                  <\/jats:sec>","DOI":"10.1093\/ndt\/gfag109","type":"journal-article","created":{"date-parts":[[2026,5,13]],"date-time":"2026-05-13T11:47:55Z","timestamp":1778672875000},"source":"Crossref","is-referenced-by-count":0,"title":["Anti-PLA2R antibodies promote endothelial pyroptosis and a procoagulant phenotype through Fc\u03b3RI signaling"],"prefix":"10.1093","author":[{"ORCID":"https:\/\/orcid.org\/0009-0007-2098-8588","authenticated-orcid":false,"given":"Cai-xia","family":"Lin","sequence":"first","affiliation":[{"name":"Renal Division, Peking University First Hospital , Beijing ,","place":["China"]},{"name":"Institute of Nephrology, Peking University , Beijing ,","place":["China"]},{"name":"Key Laboratory of Renal Disease, Ministry of Health of China , Beijing ,","place":["China"]},{"name":"Key Laboratory of Chronic Kidney Disease (CKD) Prevention and Treatment, Ministry of 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Beijing ,","place":["China"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Miao","family":"Wang","sequence":"additional","affiliation":[{"name":"Renal Division, Peking University First Hospital , Beijing ,","place":["China"]},{"name":"Institute of Nephrology, Peking University , Beijing ,","place":["China"]},{"name":"Key Laboratory of Renal Disease, Ministry of Health of China , Beijing ,","place":["China"]},{"name":"Key Laboratory of Chronic Kidney Disease (CKD) Prevention and Treatment, Ministry of Education of China , Beijing ,","place":["China"]},{"name":"Research Units of Diagnosis and Treatment of Immune-mediated Kidney Diseases, Chinese Academy of Medical Sciences , Beijing ,","place":["China"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Yu","family":"Xiao","sequence":"additional","affiliation":[{"name":"State Key Laboratory of Plant Diversity and Specialty Crops, Institute of Botany, The Chinese Academy of Sciences , Beijing 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