Malte Krakow, Johanna H Hinrichs, Judit Horvath, Hermann Pavenstädt, Marcus Brand
{"title":"SARS-CoV-2感染引发的非典型溶血性尿毒症综合征/补体介导的血栓性微血管病1例报告","authors":"Malte Krakow, Johanna H Hinrichs, Judit Horvath, Hermann Pavenstädt, Marcus Brand","doi":"10.1159/000545798","DOIUrl":null,"url":null,"abstract":"<p><strong>Introduction: </strong>Atypical hemolytic uremic syndrome (aHUS), commonly considered the prototypical form of complement-mediated thrombotic microangiopathy, is caused by dysregulated complement activation, often triggered by genetic mutations and external factors. We present a case of aHUS occurring 1 month after SARS-CoV-2 infection in a patient with a mutation in the complement factor H (CFH), a primary regulator of the alternative complement pathway.</p><p><strong>Case presentation: </strong>A 41-year-old woman with no prior conditions developed acute kidney injury, hemolytic anemia, and thrombocytopenia 1 month after SARS-CoV-2 infection. Genetic testing identified a pathogenic CFH variant (c.3572C>T), and kidney biopsy confirmed thrombotic microangiopathy. Treatment with plasma exchange, corticosteroids, and C5 inhibitors led to remission of proteinuria and improved renal function within 2 months, avoiding dialysis. Even a second SARS-CoV-2 infection 6 months after the onset of aHUS and under continuous complement C5 inhibition did not result in further kidney damage.</p><p><strong>Conclusions: </strong>Our case report is consistent with observations made by several groups that SARS-CoV-2 infection may trigger aHUS in genetically predisposed individuals. Early diagnosis and complement-targeted therapy are crucial to prevent severe outcomes.</p>","PeriodicalId":9599,"journal":{"name":"Case Reports in Nephrology and Dialysis","volume":"15 1","pages":"119-124"},"PeriodicalIF":0.7000,"publicationDate":"2025-04-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12143865/pdf/","citationCount":"0","resultStr":"{\"title\":\"Atypical Hemolytic Uremic Syndrome/Complement-Mediated Thrombotic Microangiopathy Triggered by SARS-CoV-2 Infection: A Case Report.\",\"authors\":\"Malte Krakow, Johanna H Hinrichs, Judit Horvath, Hermann Pavenstädt, Marcus Brand\",\"doi\":\"10.1159/000545798\",\"DOIUrl\":null,\"url\":null,\"abstract\":\"<p><strong>Introduction: </strong>Atypical hemolytic uremic syndrome (aHUS), commonly considered the prototypical form of complement-mediated thrombotic microangiopathy, is caused by dysregulated complement activation, often triggered by genetic mutations and external factors. We present a case of aHUS occurring 1 month after SARS-CoV-2 infection in a patient with a mutation in the complement factor H (CFH), a primary regulator of the alternative complement pathway.</p><p><strong>Case presentation: </strong>A 41-year-old woman with no prior conditions developed acute kidney injury, hemolytic anemia, and thrombocytopenia 1 month after SARS-CoV-2 infection. Genetic testing identified a pathogenic CFH variant (c.3572C>T), and kidney biopsy confirmed thrombotic microangiopathy. Treatment with plasma exchange, corticosteroids, and C5 inhibitors led to remission of proteinuria and improved renal function within 2 months, avoiding dialysis. Even a second SARS-CoV-2 infection 6 months after the onset of aHUS and under continuous complement C5 inhibition did not result in further kidney damage.</p><p><strong>Conclusions: </strong>Our case report is consistent with observations made by several groups that SARS-CoV-2 infection may trigger aHUS in genetically predisposed individuals. Early diagnosis and complement-targeted therapy are crucial to prevent severe outcomes.</p>\",\"PeriodicalId\":9599,\"journal\":{\"name\":\"Case Reports in Nephrology and Dialysis\",\"volume\":\"15 1\",\"pages\":\"119-124\"},\"PeriodicalIF\":0.7000,\"publicationDate\":\"2025-04-28\",\"publicationTypes\":\"Journal Article\",\"fieldsOfStudy\":null,\"isOpenAccess\":false,\"openAccessPdf\":\"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12143865/pdf/\",\"citationCount\":\"0\",\"resultStr\":null,\"platform\":\"Semanticscholar\",\"paperid\":null,\"PeriodicalName\":\"Case Reports in Nephrology and Dialysis\",\"FirstCategoryId\":\"1085\",\"ListUrlMain\":\"https://doi.org/10.1159/000545798\",\"RegionNum\":0,\"RegionCategory\":null,\"ArticlePicture\":[],\"TitleCN\":null,\"AbstractTextCN\":null,\"PMCID\":null,\"EPubDate\":\"2025/1/1 0:00:00\",\"PubModel\":\"eCollection\",\"JCR\":\"Q4\",\"JCRName\":\"UROLOGY & NEPHROLOGY\",\"Score\":null,\"Total\":0}","platform":"Semanticscholar","paperid":null,"PeriodicalName":"Case Reports in Nephrology and Dialysis","FirstCategoryId":"1085","ListUrlMain":"https://doi.org/10.1159/000545798","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"2025/1/1 0:00:00","PubModel":"eCollection","JCR":"Q4","JCRName":"UROLOGY & NEPHROLOGY","Score":null,"Total":0}
Atypical Hemolytic Uremic Syndrome/Complement-Mediated Thrombotic Microangiopathy Triggered by SARS-CoV-2 Infection: A Case Report.
Introduction: Atypical hemolytic uremic syndrome (aHUS), commonly considered the prototypical form of complement-mediated thrombotic microangiopathy, is caused by dysregulated complement activation, often triggered by genetic mutations and external factors. We present a case of aHUS occurring 1 month after SARS-CoV-2 infection in a patient with a mutation in the complement factor H (CFH), a primary regulator of the alternative complement pathway.
Case presentation: A 41-year-old woman with no prior conditions developed acute kidney injury, hemolytic anemia, and thrombocytopenia 1 month after SARS-CoV-2 infection. Genetic testing identified a pathogenic CFH variant (c.3572C>T), and kidney biopsy confirmed thrombotic microangiopathy. Treatment with plasma exchange, corticosteroids, and C5 inhibitors led to remission of proteinuria and improved renal function within 2 months, avoiding dialysis. Even a second SARS-CoV-2 infection 6 months after the onset of aHUS and under continuous complement C5 inhibition did not result in further kidney damage.
Conclusions: Our case report is consistent with observations made by several groups that SARS-CoV-2 infection may trigger aHUS in genetically predisposed individuals. Early diagnosis and complement-targeted therapy are crucial to prevent severe outcomes.
期刊介绍:
This peer-reviewed online-only journal publishes original case reports covering the entire spectrum of nephrology and dialysis, including genetic susceptibility, clinical presentation, diagnosis, treatment or prevention, toxicities of therapy, critical care, supportive care, quality-of-life and survival issues. The journal will also accept case reports dealing with the use of novel technologies, both in the arena of diagnosis and treatment. Supplementary material is welcomed.