Platelet hyperactivation and neutrophil extracellular traps promote thrombo-inflammation and glomerular endothelial dysfunction in diabetic kidney disease

Abstract

Introduction Diabetic kidney disease (DKD) is the cause of end-stage renal failure and contributes to morbidity and mortality worldwide. However, therapeutic options that ameliorate or reverse the progression of DKD are limited. Endothelial dysfunction, platelet hyperactivity, immune cell infiltration and glomerular filtration barrier disruption are associated with DKD. Therefore, we aimed to scrutinize the mechanistic interplay between platelets and neutrophil extracellular traps (NETs) and ensuing renal thrombo-inflammation. These insights may identify new avenues to prevent or reverse DKD.