Platelets and renal failure in the SARS-CoV-2 syndrome

Abstract

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 suggest that activated platelets may play a role in renal failure and possibly hypercoagulability status in COVID19 patients.

Keywords:

• AKI
• COVID-19
• D-Dimer
• hypercoagulable
• mean platelet volume
• renal failure
• SARS-CoV-2

Acknowledgements

This work was supported by a grant (R01HL150474 (LS) as well as the Department of Medicine, Wayne State University School of Medicine (LS).

Author Contributions

MT and ME collected clinical data and contributed in writing the manuscript. DS and AG reviewed the peripheral blood smear and contributed in writing the manuscript. SH and SD performed the statistical analysis of data. TC contributed to data interpretation and writing the manuscript. LS conceived and designed the study, participated in all areas of the research such as patients’ selection, data analysis and writing of the manuscript.

Competing Financial Interests

None of the authors of this manuscript had any financial relationship with a commercial company.

Additional information

Funding

This work was supported by the National Heart, Lung, and Blood Institute [R01HL150474].