Platelets and renal failure in the SARS-CoV-2 syndrome.
Platelets and renal failure in the SARS-CoV-2 syndrome.
复制标题
SARS-CoV-2 综合征中的血小板和肾衰竭。
DOI:
10.1080/09537104.2020.1817361
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发表时间:
2021-01-02
期刊:
影响因子:
3.3
通讯作者:
Samavati L
中科院分区:
文献类型:
--
作者:
Taha M;Sano D;Hanoudi S;Esber Z;Elahi M;Gabali A;Chopra T;Draghici S;Samavati L
The coronavirus disease 19 (COVID-19) is a highly transmittable viral infection caused by the severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2). SARS‐CoV‐2 utilizes metallocarboxyl peptidase angiotensin receptor (ACE) 2 to gain entry into human cells. Activation of several proteases facilitates the interaction of viral spike proteins (S1) and ACE2 receptor. This leads to cleavage of host ACE2 receptors. ACE2 activity counterbalances the angiotensin II effect, its loss may lead to elevated angiotensin II levels with modulation of platelet function, size and activity. COVID-19 disease encompasses a spectrum of systemic involvement far beyond respiratory failure alone. Several features of this disease, including the etiology of acute kidney injury (AKI) and the hypercoagulable state, remain poorly understood. Here, we show that there is a high incidence of AKI (81%) in the critically ill adults with COVID-19 in the setting of elevated D-dimer, elevated ferritin, C reactive protein (CRP) and lactate dehydrogenase (LDH) levels. Strikingly, there were unique features of platelets in these patients, including larger, more granular platelets and a higher mean platelet volume (MPV). There was a significant correlation between measured D-dimer levels and MVP; but a negative correlation between MPV and glomerular filtration rates (GFR) in critically ill cohort. Our data suggests that activated platelets may play a role in renal failure and possibly hypercoagulability status in COVID19 patients.
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