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The pathogenesis of hyperuricemia is primarily delineated into two pathophysiological mechanisms: hyperproduction of uric acid and defective renal excretion

Hijacking of ACE2 by the viral spike and its internalization, may lead to a shift from the protective to the deleterious axis of the RAAS, contributing to the vascular complications observed during COVID-19, such as endothelial cell inflammation 9,10,11

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