Complement system is overactivated in patients with IgA nephropathy after COVID-19
IgA nephropathy (IgAN), which has been confirmed as a complement mediated autoimmune disease, is also one form of glomerulonephritis associated with COVID-19. Here, we aim to investigate the clinical and immunological characteristics of patients with IgAN after COVID-19. The level of plasma level of...
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| Veröffentlicht in: | Clinical immunology (Orlando, Fla.) Fla.), 2024-06, Vol.263, p.110232, Article 110232 |
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| container_title | Clinical immunology (Orlando, Fla.) |
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| creator | Guo, Wei-yi Wang, Guo-qin Kong, Ling-qiang Sun, Li-jun Xu, Xiao-yi Cheng, Wen-rong Dong, Hong-rui Cheng, Hong |
| description | IgA nephropathy (IgAN), which has been confirmed as a complement mediated autoimmune disease, is also one form of glomerulonephritis associated with COVID-19. Here, we aim to investigate the clinical and immunological characteristics of patients with IgAN after COVID-19. The level of plasma level of C5a (p |
| doi_str_mv | 10.1016/j.clim.2024.110232 |
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Here, we aim to investigate the clinical and immunological characteristics of patients with IgAN after COVID-19. The level of plasma level of C5a (p < 0.001), soluble C5b-9 (p = 0.018), FHR5 (p < 0.001) were all significantly higher in Group CoV (33 patients with renal biopsy-proven IgAN experienced COVID-19) compared with Group non-CoV (44 patients with IgAN without COVID-19), respectively. Compared with Group non-CoV, the intensity of glomerular C4d (p = 0.017) and MAC deposition (p < 0.001) and Gd-IgA1 deposition (p = 0.005) were much stronger in Group CoV. Our finding revealed that for IgAN after COVID-19, mucosal immune responses to SARS-CoV-2 infection may result in the overactivation of systemic and renal local complement system, and increased glomerular deposition of Gd-IgA1, which may lead to renal dysfunction and promote renal progression in IgAN patients.</description><identifier>ISSN: 1521-6616</identifier><identifier>ISSN: 1521-7035</identifier><identifier>EISSN: 1521-7035</identifier><identifier>DOI: 10.1016/j.clim.2024.110232</identifier><identifier>PMID: 38701960</identifier><language>eng</language><publisher>United States: Elsevier Inc</publisher><subject>Complement system ; COVID-19 ; Gd-IgA1 ; IgA nephropathy</subject><ispartof>Clinical immunology (Orlando, Fla.), 2024-06, Vol.263, p.110232, Article 110232</ispartof><rights>2024 The Authors</rights><rights>Copyright © 2024. Published by Elsevier Inc.</rights><rights>Copyright © 2024 The Authors. Published by Elsevier Inc. 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Here, we aim to investigate the clinical and immunological characteristics of patients with IgAN after COVID-19. The level of plasma level of C5a (p < 0.001), soluble C5b-9 (p = 0.018), FHR5 (p < 0.001) were all significantly higher in Group CoV (33 patients with renal biopsy-proven IgAN experienced COVID-19) compared with Group non-CoV (44 patients with IgAN without COVID-19), respectively. Compared with Group non-CoV, the intensity of glomerular C4d (p = 0.017) and MAC deposition (p < 0.001) and Gd-IgA1 deposition (p = 0.005) were much stronger in Group CoV. Our finding revealed that for IgAN after COVID-19, mucosal immune responses to SARS-CoV-2 infection may result in the overactivation of systemic and renal local complement system, and increased glomerular deposition of Gd-IgA1, which may lead to renal dysfunction and promote renal progression in IgAN patients.</description><subject>Complement system</subject><subject>COVID-19</subject><subject>Gd-IgA1</subject><subject>IgA nephropathy</subject><issn>1521-6616</issn><issn>1521-7035</issn><issn>1521-7035</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2024</creationdate><recordtype>article</recordtype><recordid>eNp9kMtKAzEUhoMo3l_AhWTpZmouk7QBN1JvBUEQdRvS5MSmzHTGJK307U1pdWk2Ced8_w_5ELqgZEAJldfzgW1CO2CE1QNKCeNsDx1TwWg1JFzs795SUnmETlKaE0IEY_IQHfHRkFAlyTF6HXdt30ALi4zTOmVocUi4W0E0NoeVyeBwWODe5FCQhL9DnuHJ5y1eQD-LXZnP1tj4DBGPXz4mdxVVZ-jAmybB-e4-Re8P92_jp-r55XEyvn2uLBc0V6CUIMzIGpS3UgwFdyNHVDlMiGntHTArPHguRkNn6qkVDlxtytrXU889P0VX294-dl9LSFm3IVloGrOAbpk0J4IorhSVBWVb1MYupQhe9zG0Jq41JXrjUs_1xqXeuNRblyV0uetfTltwf5FfeQW42QJQfrkKEHWyxZIFFyLYrF0X_uv_AVzNhPY</recordid><startdate>20240601</startdate><enddate>20240601</enddate><creator>Guo, Wei-yi</creator><creator>Wang, Guo-qin</creator><creator>Kong, Ling-qiang</creator><creator>Sun, Li-jun</creator><creator>Xu, Xiao-yi</creator><creator>Cheng, Wen-rong</creator><creator>Dong, Hong-rui</creator><creator>Cheng, Hong</creator><general>Elsevier Inc</general><scope>6I.</scope><scope>AAFTH</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>7X8</scope></search><sort><creationdate>20240601</creationdate><title>Complement system is overactivated in patients with IgA nephropathy after COVID-19</title><author>Guo, Wei-yi ; Wang, Guo-qin ; Kong, Ling-qiang ; Sun, Li-jun ; Xu, Xiao-yi ; Cheng, Wen-rong ; Dong, Hong-rui ; Cheng, Hong</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c351t-e99502a64e9fc65753d8d09999255b4fde2c5fef3587da4bc5ded4a992f4bf3f3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2024</creationdate><topic>Complement system</topic><topic>COVID-19</topic><topic>Gd-IgA1</topic><topic>IgA nephropathy</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Guo, Wei-yi</creatorcontrib><creatorcontrib>Wang, Guo-qin</creatorcontrib><creatorcontrib>Kong, Ling-qiang</creatorcontrib><creatorcontrib>Sun, Li-jun</creatorcontrib><creatorcontrib>Xu, Xiao-yi</creatorcontrib><creatorcontrib>Cheng, Wen-rong</creatorcontrib><creatorcontrib>Dong, Hong-rui</creatorcontrib><creatorcontrib>Cheng, Hong</creatorcontrib><collection>ScienceDirect Open Access Titles</collection><collection>Elsevier:ScienceDirect:Open Access</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>MEDLINE - Academic</collection><jtitle>Clinical immunology (Orlando, Fla.)</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Guo, Wei-yi</au><au>Wang, Guo-qin</au><au>Kong, Ling-qiang</au><au>Sun, Li-jun</au><au>Xu, Xiao-yi</au><au>Cheng, Wen-rong</au><au>Dong, Hong-rui</au><au>Cheng, Hong</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Complement system is overactivated in patients with IgA nephropathy after COVID-19</atitle><jtitle>Clinical immunology (Orlando, Fla.)</jtitle><addtitle>Clin Immunol</addtitle><date>2024-06-01</date><risdate>2024</risdate><volume>263</volume><spage>110232</spage><pages>110232-</pages><artnum>110232</artnum><issn>1521-6616</issn><issn>1521-7035</issn><eissn>1521-7035</eissn><abstract>IgA nephropathy (IgAN), which has been confirmed as a complement mediated autoimmune disease, is also one form of glomerulonephritis associated with COVID-19. Here, we aim to investigate the clinical and immunological characteristics of patients with IgAN after COVID-19. The level of plasma level of C5a (p < 0.001), soluble C5b-9 (p = 0.018), FHR5 (p < 0.001) were all significantly higher in Group CoV (33 patients with renal biopsy-proven IgAN experienced COVID-19) compared with Group non-CoV (44 patients with IgAN without COVID-19), respectively. Compared with Group non-CoV, the intensity of glomerular C4d (p = 0.017) and MAC deposition (p < 0.001) and Gd-IgA1 deposition (p = 0.005) were much stronger in Group CoV. Our finding revealed that for IgAN after COVID-19, mucosal immune responses to SARS-CoV-2 infection may result in the overactivation of systemic and renal local complement system, and increased glomerular deposition of Gd-IgA1, which may lead to renal dysfunction and promote renal progression in IgAN patients.</abstract><cop>United States</cop><pub>Elsevier Inc</pub><pmid>38701960</pmid><doi>10.1016/j.clim.2024.110232</doi><oa>free_for_read</oa></addata></record> |
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| subjects | Complement system COVID-19 Gd-IgA1 IgA nephropathy |
| title | Complement system is overactivated in patients with IgA nephropathy after COVID-19 |
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