Neutrophil Extracellular Traps Aggravate Injury in Complement-Mediated Thrombotic Microangiopathy
Key Points
The central aim is to understand how neutrophil extracellular traps (NETs) contribute to organ injury in complement-mediated thrombotic microangiopathy (TMA).
Assessment of NETs biomarkers in patients with complement-mediated TMA.
Evaluation of CD59 shedding from human renal glomerular endothelial cells (HRGECs).
Analysis of the relationship between NETs and complement activation as well as coagulation processes.
Increased levels of NETs biomarkers were observed in cases of complement-mediated TMA.
NETs contributed to organ injury by shedding CD59 from HRGECs, which enhanced complement activation.
NETs were linked to the activation of coagulation pathways.
Abstract
Levels of NETs biomarkers increased in complement-mediated TMA and drove multi-organ injury by shedding CD59 from HRGECs to enhance complement activation and participate in coagulation activation.