Atypical hemolytic uremic syndrome: a case report and review of thrombotic mechanisms

Abstract Using specific clinical analyses, including genetic, hemolytic, blood, and disease manifestations, leads to a unique hypothesis about our patient’s atypical hemolytic uremic syndrome pathophysiology. Notably, a novel C3 defect, in addition to a common factor B mutation, leads to doubt over...

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Main Author: George N. Zsidisin
Format: Article
Language:English
Published: Springer 2025-04-01
Series:Journal of Rare Diseases
Subjects:
Online Access:https://doi.org/10.1007/s44162-025-00072-3
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author George N. Zsidisin
author_facet George N. Zsidisin
author_sort George N. Zsidisin
collection DOAJ
description Abstract Using specific clinical analyses, including genetic, hemolytic, blood, and disease manifestations, leads to a unique hypothesis about our patient’s atypical hemolytic uremic syndrome pathophysiology. Notably, a novel C3 defect, in addition to a common factor B mutation, leads to doubt over current theories of alternative complement overactivation and further drives focus onto the thrombotic nature of the disease. We propose a pathology of defective platelet-leukocyte-endothelial adhesions, leading to poor leukocyte extravasation.
format Article
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spelling doaj-art-2b0b807e4db54ba2aa6d9d4997b0360d2025-08-20T03:03:20ZengSpringerJournal of Rare Diseases2731-085X2025-04-01411610.1007/s44162-025-00072-3Atypical hemolytic uremic syndrome: a case report and review of thrombotic mechanismsGeorge N. Zsidisin0Clinical Institute of Fundeni Nephrology Department, Carol Davila University of Medicine and PharmacyAbstract Using specific clinical analyses, including genetic, hemolytic, blood, and disease manifestations, leads to a unique hypothesis about our patient’s atypical hemolytic uremic syndrome pathophysiology. Notably, a novel C3 defect, in addition to a common factor B mutation, leads to doubt over current theories of alternative complement overactivation and further drives focus onto the thrombotic nature of the disease. We propose a pathology of defective platelet-leukocyte-endothelial adhesions, leading to poor leukocyte extravasation.https://doi.org/10.1007/s44162-025-00072-3Atypical hemolytic uremic syndromePlatelet activationThrombinPhagocytosisNETosisComplement proteins
spellingShingle George N. Zsidisin
Atypical hemolytic uremic syndrome: a case report and review of thrombotic mechanisms
Journal of Rare Diseases
Atypical hemolytic uremic syndrome
Platelet activation
Thrombin
Phagocytosis
NETosis
Complement proteins
title Atypical hemolytic uremic syndrome: a case report and review of thrombotic mechanisms
title_full Atypical hemolytic uremic syndrome: a case report and review of thrombotic mechanisms
title_fullStr Atypical hemolytic uremic syndrome: a case report and review of thrombotic mechanisms
title_full_unstemmed Atypical hemolytic uremic syndrome: a case report and review of thrombotic mechanisms
title_short Atypical hemolytic uremic syndrome: a case report and review of thrombotic mechanisms
title_sort atypical hemolytic uremic syndrome a case report and review of thrombotic mechanisms
topic Atypical hemolytic uremic syndrome
Platelet activation
Thrombin
Phagocytosis
NETosis
Complement proteins
url https://doi.org/10.1007/s44162-025-00072-3
work_keys_str_mv AT georgenzsidisin atypicalhemolyticuremicsyndromeacasereportandreviewofthromboticmechanisms