Year: 2025
Type: article
Study design: Case Report
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.
Source: Journal of Rare Diseases
Author: George N. Zsidisin
Language: English
Subfield: Immunology
Field: Immunology and Microbiology
Domain: Life Sciences
Open Access status: diamond
OpenAlex ID: W4409162886
