PROJECT EXECUTIVE SUMMARY
The coronavirus disease 2019 (COVID-19) caused by the severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) produced a pandemic on March 2020 by affecting more than 6.8 million people with more than 5.8 % deaths. SARS-CoV-2 infection is produced by binding to angiotensin-converting enzyme, which among other sites is highly expressed in the endothelial cells of the blood vessels, pericytes and the heart, as well as in renal podocytes and proximal tubular epithelial cells. SARS-COV-2 and cardiovascular disease (CVD) are interconnected by risk factors association with an increased incidence of the disease and by determining de novo cardiac complications. At the same time, COVID-19 disease can lead to acute kidney injury directly, or due to sepsis, multi-organ failure and shock. Therefore, the preexistence of both CVD and chronic kidney disease (CKD) is associated with a higher risk of population, following COVID-19 SARS-CoV-2 infection, with focus on the endothelial dysfunction as compared to a control group of severe disease and worse prognosis. Taking all this into account, the main aim of study is to holistically assess the CV risk in a CKD population, following COVID-19 SARS-CoV-2 infection, with focus on the endothelial dysfunction as compared to a control group of matched CKD patients, by using clinical evaluation, flow-mediated dilatation, carotid-femoral pulse wave velocity, intima-media thickness, echocardiographic parameters, lung ultrasound, bioimpedance spectroscopy and a series of novel biomarkers, in order to determine the long-term impact of this disease on CV and renal outcomes.