Acute Kidney Injury in COVID-19: Emerging Evidence of a Dist
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The most common reported reasons for intensive care unit admission for patients with severe COVID-19 are either hypoxemic respiratory failure leading to mechanical ventilation or hypotension requiring vasopressor support. Data on AKI are either lacking or only reporting incidence on the basis of case series and retrospective studies. In this Perspective, authors emphasize that AKI can be a severe complication of COVID-19 and highlight the importance of assessing, defining, and reporting the course of AKI.

Innate immunity and coagulation pathways are intricately linked. COVID-19–associated macrophage activation, hyperferritinemia, cytokine storm, and release of pathogen-associated molecular patterns and damage-associated molecular proteins can result in release of tissue factor and activation of coagulation factors that create a predisposition to hypercoagulability.

SARS-CoV-2 may also target lymphocytes as they express ACE2, leading to lymphocyte activation and, consequently, activation-induced cell death than can result in lymphopenia of both CD4+ and CD8+ T cells. Further, procoagulation pathways and complement systems can activate each other.

Detailed studies to decipher the nature of coagulation dysfunction, microangiopathy, and potential role for innate immune and complement pathways are required to gain further insights regarding kidney pathology in COVID-19.