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<p>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.</p>

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

  • 期刊论文

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  • 发表日期：

    2025年4月3日

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  • George N. Zsidisin

摘要

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.