This was confirmed in a newly published letter by Lippi and coworkers in Clinical Chemistry and Laboratory Medicine. The authors reviewed various studies exploring suPAR concentrations in COVID-19 patients.

suPAR was found to be increased by 55% in patients with various forms of critical illness compared to those without.

The results suggest that the measurement of suPAR in COVID-19 patients may represent a valuable tool for improving risk stratification accuracy, helping to predict the risk of developing severe consequences of a SARS-CoV-2 infection, especially acute kidney injury (AKI), along with micro- and macro-thrombosis.

Increased suPAR concentration has been associated with enhanced extra-mitochondrial enzymatic oxidation and oxidative stress in renal cells, which may act in synergy with the direct kidney cell injury caused by SARS-CoV-2 and indirect injury triggered by microthrombi in the renal vasculature, thus augmenting the risk of developing AKI. It has also been suggested that enhanced suPAR release in the bloodstream may contribute to reduce plasmin generation by competitive inhibition of urokinase-type plasminogen activator (uPA) at cell surface. This would ultimately promote the development of a hypofibrinolytic condition, a characteristic component of the hypercoagulable state that is common in patients with severe COVID-19 and would finally converge to synergically exacerbate the severity of thrombosis.

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ViroGates A/S published this content on 15 June 2021 and is solely responsible for the information contained therein. Distributed by Public, unedited and unaltered, on 15 June 2021 14:39:08 UTC.