A study of kidney disease patients found that a specific antibody linked to membranous nephropathy triggers blood vessel cells to enter a self-destructive inflammatory state, raising the risk of dangerous blood clots.
1
Anti-PLA2R antibody levels above 92 RU/mL were associated with higher thromboembolic risk in membranous nephropathy patients (n=45 cases vs. controls).
2
In lab-grown human blood vessel cells, anti-PLA2R antibodies triggered pyroptosis (inflammatory cell death) and upregulated tissue factor, ICAM-1, and PAI-1 via FcγRI signaling — effects blocked by FcγRI silencing.
3
Complement proteins C3a and C5a further amplified the procoagulant response via their respective receptors, and receptor antagonists reversed plasma-induced effects.
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