Atypical hemolytic uremic syndrome with a C3 variant following COVID-19: a case report
Atypical hemolytic uremic syndrome (aHUS) is a form of thrombotic microangiopathy (TMA) characterized by the triad of microangiopathic hemolytic anemia, thrombocytopenia, and acute kidney injury, and is caused by overactivation of the alternative complement pathway. A 13-year-old Japanese boy with a...
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Frontiers Media S.A.
2025-01-01
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| Series: | Frontiers in Pediatrics |
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| Online Access: | https://www.frontiersin.org/articles/10.3389/fped.2025.1507727/full |
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| author | Masato Ando Kazuo Kubota Kazuo Kubota Saori Kadowaki Minako Kawamoto Norio Kawamoto Haruka Okamoto Soichiro Nagaya Yuki Miwa Hidenori Ohnishi Hidenori Ohnishi |
| author_facet | Masato Ando Kazuo Kubota Kazuo Kubota Saori Kadowaki Minako Kawamoto Norio Kawamoto Haruka Okamoto Soichiro Nagaya Yuki Miwa Hidenori Ohnishi Hidenori Ohnishi |
| author_sort | Masato Ando |
| collection | DOAJ |
| description | Atypical hemolytic uremic syndrome (aHUS) is a form of thrombotic microangiopathy (TMA) characterized by the triad of microangiopathic hemolytic anemia, thrombocytopenia, and acute kidney injury, and is caused by overactivation of the alternative complement pathway. A 13-year-old Japanese boy with an unremarkable medical history developed symptoms of TMA following coronavirus disease 2019 (COVID-19) infection with mild respiratory symptoms. He was eventually diagnosed with aHUS with a gain-of-function C3 variant. He improved with supportive therapy and plasma exchange, and did not require anti-C5 antibody therapy. In the literature, more than 20 cases of de novo or relapsed aHUS have been described following COVID-19. It has been shown that the complement lectin pathway can be activated by the severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) spike and N proteins, and the alternative pathway can be activated by the SARS-CoV-2 spike protein. The current case highlights the possibility that COVID-19, even when respiratory symptoms are not severe, can trigger aHUS. |
| format | Article |
| id | doaj-art-fb3ca787aa4e471f9bfb300bafdb6b2e |
| institution | Kabale University |
| issn | 2296-2360 |
| language | English |
| publishDate | 2025-01-01 |
| publisher | Frontiers Media S.A. |
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| series | Frontiers in Pediatrics |
| spelling | doaj-art-fb3ca787aa4e471f9bfb300bafdb6b2e2025-01-23T06:56:27ZengFrontiers Media S.A.Frontiers in Pediatrics2296-23602025-01-011310.3389/fped.2025.15077271507727Atypical hemolytic uremic syndrome with a C3 variant following COVID-19: a case reportMasato Ando0Kazuo Kubota1Kazuo Kubota2Saori Kadowaki3Minako Kawamoto4Norio Kawamoto5Haruka Okamoto6Soichiro Nagaya7Yuki Miwa8Hidenori Ohnishi9Hidenori Ohnishi10Department of Pediatrics, Graduate School of Medicine, Gifu University, Gifu, JapanDepartment of Pediatrics, Graduate School of Medicine, Gifu University, Gifu, JapanClinical Genetics Center, Gifu University Hospital, Gifu, JapanDepartment of Pediatrics, Graduate School of Medicine, Gifu University, Gifu, JapanDepartment of Pediatrics, Graduate School of Medicine, Gifu University, Gifu, JapanDepartment of Pediatrics, Graduate School of Medicine, Gifu University, Gifu, JapanGifu University Advanced Critical Care Center, Gifu, JapanGifu University Advanced Critical Care Center, Gifu, JapanDepartment of Pediatrics, Graduate School of Medicine, Gifu University, Gifu, JapanDepartment of Pediatrics, Graduate School of Medicine, Gifu University, Gifu, JapanClinical Genetics Center, Gifu University Hospital, Gifu, JapanAtypical hemolytic uremic syndrome (aHUS) is a form of thrombotic microangiopathy (TMA) characterized by the triad of microangiopathic hemolytic anemia, thrombocytopenia, and acute kidney injury, and is caused by overactivation of the alternative complement pathway. A 13-year-old Japanese boy with an unremarkable medical history developed symptoms of TMA following coronavirus disease 2019 (COVID-19) infection with mild respiratory symptoms. He was eventually diagnosed with aHUS with a gain-of-function C3 variant. He improved with supportive therapy and plasma exchange, and did not require anti-C5 antibody therapy. In the literature, more than 20 cases of de novo or relapsed aHUS have been described following COVID-19. It has been shown that the complement lectin pathway can be activated by the severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) spike and N proteins, and the alternative pathway can be activated by the SARS-CoV-2 spike protein. The current case highlights the possibility that COVID-19, even when respiratory symptoms are not severe, can trigger aHUS.https://www.frontiersin.org/articles/10.3389/fped.2025.1507727/fullatypical hemolytic uremic syndromeGOF C3 variantsevere acute respiratory syndrome coronavirus 2alternative complement pathwayinborn errors of immunity |
| spellingShingle | Masato Ando Kazuo Kubota Kazuo Kubota Saori Kadowaki Minako Kawamoto Norio Kawamoto Haruka Okamoto Soichiro Nagaya Yuki Miwa Hidenori Ohnishi Hidenori Ohnishi Atypical hemolytic uremic syndrome with a C3 variant following COVID-19: a case report Frontiers in Pediatrics atypical hemolytic uremic syndrome GOF C3 variant severe acute respiratory syndrome coronavirus 2 alternative complement pathway inborn errors of immunity |
| title | Atypical hemolytic uremic syndrome with a C3 variant following COVID-19: a case report |
| title_full | Atypical hemolytic uremic syndrome with a C3 variant following COVID-19: a case report |
| title_fullStr | Atypical hemolytic uremic syndrome with a C3 variant following COVID-19: a case report |
| title_full_unstemmed | Atypical hemolytic uremic syndrome with a C3 variant following COVID-19: a case report |
| title_short | Atypical hemolytic uremic syndrome with a C3 variant following COVID-19: a case report |
| title_sort | atypical hemolytic uremic syndrome with a c3 variant following covid 19 a case report |
| topic | atypical hemolytic uremic syndrome GOF C3 variant severe acute respiratory syndrome coronavirus 2 alternative complement pathway inborn errors of immunity |
| url | https://www.frontiersin.org/articles/10.3389/fped.2025.1507727/full |
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