Christof Aigner, Martina Gaggl, Sophie Schmidt, Renate Kain, Nicolas Kozakowski, André Oszwald, Zoltán Prohászka, Raute Sunder-Plassmann, Alice Schmidt, Gere Sunder-Plassmann
{"title":"COVID-19 大流行期间新出现的补体介导的血栓性微血管病。","authors":"Christof Aigner, Martina Gaggl, Sophie Schmidt, Renate Kain, Nicolas Kozakowski, André Oszwald, Zoltán Prohászka, Raute Sunder-Plassmann, Alice Schmidt, Gere Sunder-Plassmann","doi":"10.1159/000541938","DOIUrl":null,"url":null,"abstract":"<p><strong>Introduction: </strong>The coronavirus disease-19 (COVID-19) is caused by the severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2). The virus is alleged to enable a proinflammatory state that leads to the activation of the coagulation and the complement cascade. In this study, we aimed to establish the impact of the COVID-19 pandemic on patients with new onset of cTMA/aHUS in the Vienna TMA cohort and whether COVID-19 or SARS-CoV-2 vaccinations would pose a greater risk of initial manifestation of cTMA/aHUS.</p><p><strong>Methods: </strong>We used the Vienna TMA cohort database to examine the prevalence of COVID-19-related and of SARS-CoV-2 vaccination-related aHUS/cTMA during the first 3 years of the COVID-19 pandemic in a large single-centre cohort.</p><p><strong>Results: </strong>Between March 2020 and May 2023, a total of 7 patients experienced their first aHUS/cTMA episode. No patient experienced a TMA relapse or more than one episode during the follow-up period. Three TMA episodes were attributable to either COVID-19 (n = 1; 33%) or SARS-CoV-2 vaccination (n = 2; 66%), respectively. All 3 patients had systemic signs of TMA, and TMA was confirmed by kidney biopsy in all cases. Among the 7 patients, we recorded five infections that triggered one TMA episode (20%) and 19 vaccinations triggered two TMA episodes (10%; p = 0.52, odds ratio 0.47; 95% CI: 0.04-8.39).</p><p><strong>Conclusion: </strong>We speculate that both SARS-CoV-2 vaccinations and COVID-19 episodes can represent a triggering factor for aHUS/cTMA episodes in (genetically) vulnerable individuals. However, COVID-19 might have a stronger association and might be a stronger trigger than the SARS-CoV-2 vaccines. The incidence of new aHUS cases did not differ from the pre-pandemic era in a large tertiary care centre cohort.</p>","PeriodicalId":17813,"journal":{"name":"Kidney & blood pressure research","volume":" ","pages":"970-977"},"PeriodicalIF":2.3000,"publicationDate":"2024-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":"{\"title\":\"New-Onset Complement-Mediated Thrombotic Microangiopathy during the COVID-19 Pandemic.\",\"authors\":\"Christof Aigner, Martina Gaggl, Sophie Schmidt, Renate Kain, Nicolas Kozakowski, André Oszwald, Zoltán Prohászka, Raute Sunder-Plassmann, Alice Schmidt, Gere Sunder-Plassmann\",\"doi\":\"10.1159/000541938\",\"DOIUrl\":null,\"url\":null,\"abstract\":\"<p><strong>Introduction: </strong>The coronavirus disease-19 (COVID-19) is caused by the severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2). The virus is alleged to enable a proinflammatory state that leads to the activation of the coagulation and the complement cascade. In this study, we aimed to establish the impact of the COVID-19 pandemic on patients with new onset of cTMA/aHUS in the Vienna TMA cohort and whether COVID-19 or SARS-CoV-2 vaccinations would pose a greater risk of initial manifestation of cTMA/aHUS.</p><p><strong>Methods: </strong>We used the Vienna TMA cohort database to examine the prevalence of COVID-19-related and of SARS-CoV-2 vaccination-related aHUS/cTMA during the first 3 years of the COVID-19 pandemic in a large single-centre cohort.</p><p><strong>Results: </strong>Between March 2020 and May 2023, a total of 7 patients experienced their first aHUS/cTMA episode. No patient experienced a TMA relapse or more than one episode during the follow-up period. Three TMA episodes were attributable to either COVID-19 (n = 1; 33%) or SARS-CoV-2 vaccination (n = 2; 66%), respectively. All 3 patients had systemic signs of TMA, and TMA was confirmed by kidney biopsy in all cases. Among the 7 patients, we recorded five infections that triggered one TMA episode (20%) and 19 vaccinations triggered two TMA episodes (10%; p = 0.52, odds ratio 0.47; 95% CI: 0.04-8.39).</p><p><strong>Conclusion: </strong>We speculate that both SARS-CoV-2 vaccinations and COVID-19 episodes can represent a triggering factor for aHUS/cTMA episodes in (genetically) vulnerable individuals. However, COVID-19 might have a stronger association and might be a stronger trigger than the SARS-CoV-2 vaccines. The incidence of new aHUS cases did not differ from the pre-pandemic era in a large tertiary care centre cohort.</p>\",\"PeriodicalId\":17813,\"journal\":{\"name\":\"Kidney & blood pressure research\",\"volume\":\" \",\"pages\":\"970-977\"},\"PeriodicalIF\":2.3000,\"publicationDate\":\"2024-01-01\",\"publicationTypes\":\"Journal Article\",\"fieldsOfStudy\":null,\"isOpenAccess\":false,\"openAccessPdf\":\"\",\"citationCount\":\"0\",\"resultStr\":null,\"platform\":\"Semanticscholar\",\"paperid\":null,\"PeriodicalName\":\"Kidney & blood pressure research\",\"FirstCategoryId\":\"3\",\"ListUrlMain\":\"https://doi.org/10.1159/000541938\",\"RegionNum\":4,\"RegionCategory\":\"医学\",\"ArticlePicture\":[],\"TitleCN\":null,\"AbstractTextCN\":null,\"PMCID\":null,\"EPubDate\":\"2024/10/22 0:00:00\",\"PubModel\":\"Epub\",\"JCR\":\"Q2\",\"JCRName\":\"PERIPHERAL VASCULAR DISEASE\",\"Score\":null,\"Total\":0}","platform":"Semanticscholar","paperid":null,"PeriodicalName":"Kidney & blood pressure research","FirstCategoryId":"3","ListUrlMain":"https://doi.org/10.1159/000541938","RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"2024/10/22 0:00:00","PubModel":"Epub","JCR":"Q2","JCRName":"PERIPHERAL VASCULAR DISEASE","Score":null,"Total":0}
New-Onset Complement-Mediated Thrombotic Microangiopathy during the COVID-19 Pandemic.
Introduction: The coronavirus disease-19 (COVID-19) is caused by the severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2). The virus is alleged to enable a proinflammatory state that leads to the activation of the coagulation and the complement cascade. In this study, we aimed to establish the impact of the COVID-19 pandemic on patients with new onset of cTMA/aHUS in the Vienna TMA cohort and whether COVID-19 or SARS-CoV-2 vaccinations would pose a greater risk of initial manifestation of cTMA/aHUS.
Methods: We used the Vienna TMA cohort database to examine the prevalence of COVID-19-related and of SARS-CoV-2 vaccination-related aHUS/cTMA during the first 3 years of the COVID-19 pandemic in a large single-centre cohort.
Results: Between March 2020 and May 2023, a total of 7 patients experienced their first aHUS/cTMA episode. No patient experienced a TMA relapse or more than one episode during the follow-up period. Three TMA episodes were attributable to either COVID-19 (n = 1; 33%) or SARS-CoV-2 vaccination (n = 2; 66%), respectively. All 3 patients had systemic signs of TMA, and TMA was confirmed by kidney biopsy in all cases. Among the 7 patients, we recorded five infections that triggered one TMA episode (20%) and 19 vaccinations triggered two TMA episodes (10%; p = 0.52, odds ratio 0.47; 95% CI: 0.04-8.39).
Conclusion: We speculate that both SARS-CoV-2 vaccinations and COVID-19 episodes can represent a triggering factor for aHUS/cTMA episodes in (genetically) vulnerable individuals. However, COVID-19 might have a stronger association and might be a stronger trigger than the SARS-CoV-2 vaccines. The incidence of new aHUS cases did not differ from the pre-pandemic era in a large tertiary care centre cohort.
期刊介绍:
This journal comprises both clinical and basic studies at the interface of nephrology, hypertension and cardiovascular research. The topics to be covered include the structural organization and biochemistry of the normal and diseased kidney, the molecular biology of transporters, the physiology and pathophysiology of glomerular filtration and tubular transport, endothelial and vascular smooth muscle cell function and blood pressure control, as well as water, electrolyte and mineral metabolism. Also discussed are the (patho)physiology and (patho) biochemistry of renal hormones, the molecular biology, genetics and clinical course of renal disease and hypertension, the renal elimination, action and clinical use of drugs, as well as dialysis and transplantation. Featuring peer-reviewed original papers, editorials translating basic science into patient-oriented research and disease, in depth reviews, and regular special topic sections, ''Kidney & Blood Pressure Research'' is an important source of information for researchers in nephrology and cardiovascular medicine.