Excessive complement activation plays a crucial role in the pathogenesis of atypical hemolytic uremic syndrome (aHUS). However, its involvement in Shiga Toxin-Producing Escherichia coli– Associated Hemolytic Uremic Syndrome (STEC-HUS) remains uncertain. This study aimed to investigate the potential role of complement activation products and rare variants or disease risk polymorphisms in complement alternative pathway components in the pathogenesis of STECHUS.
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Vallés et al. (2024) studied this question.
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