医学
内皮功能障碍
动脉硬化
血管收缩
内皮素受体
血管炎
内科学
显微镜下多血管炎
内皮
免疫学
纤溶
抗中性粒细胞胞浆抗体
心脏病学
受体
疾病
血压
标识
DOI:10.1016/j.kint.2022.08.029
摘要
In this issue, Farrah et al. report clinical investigations in patients with antineutrophil cytoplasmic antibody–associated vasculitis (AAV). They demonstrate that endothelium-dependent vasodilatation, fibrinolytic capacity, and monocyte-dependent endothelin-1 clearance are reduced in patients with AAV, whereas circulating levels of endothelin-1 and vascular stiffness are increased. Acute infusion of an endothelin ETA receptor antagonist reduced vasoconstriction and arterial stiffness. This Commentary discusses biological insights and clinical implications of this study. In this issue, Farrah et al. report clinical investigations in patients with antineutrophil cytoplasmic antibody–associated vasculitis (AAV). They demonstrate that endothelium-dependent vasodilatation, fibrinolytic capacity, and monocyte-dependent endothelin-1 clearance are reduced in patients with AAV, whereas circulating levels of endothelin-1 and vascular stiffness are increased. Acute infusion of an endothelin ETA receptor antagonist reduced vasoconstriction and arterial stiffness. This Commentary discusses biological insights and clinical implications of this study. Arterial stiffness, endothelial dysfunction and impaired fibrinolysis are pathogenic mechanisms contributing to cardiovascular risk in ANCA-associated vasculitisKidney InternationalVol. 102Issue 5PreviewCardiovascular disease is a complication of systemic inflammatory diseases including anti-neutrophil cytoplasm antibody-associated vasculitis (AAV). The mechanisms of cardiovascular morbidity in AAV are poorly understood, and risk-reduction strategies are lacking. Therefore, in a series of double-blind, randomized case-control forearm plethysmography and crossover systemic interventional studies, we examined arterial stiffness and endothelial function in patients with AAV in long-term disease remission and in matched healthy volunteers (32 each group). Full-Text PDF Open Access
科研通智能强力驱动
Strongly Powered by AbleSci AI