Fig. 1

Theoretical model of kidney-lung interaction during COVID-19. We postulate that SARS-CoV2 enters a lung and perhaps a kidney using ACE2 as a main entry point and TMPRSS2 for proteolitic cleavage (priming) of SARS-CoV2-ACE2 complex to increase the infection rate. Ensuing injury (“second hit”), such as ventilation injury and AKI (local tissue inflammation) can alter the expression of these two genes and change response to the infection. The left panel, therefore, represents ventilation injury and right panel represents AKI. Expression values for ACE2 and TMPRSS2 genes are depicted in closed boxes and are taken from Table 1. Solid boxes/lines represent direct effects of an injury, and dashed boxes/lines represent distant genomic effects at 6 h after the injury. Aside from ACE2/TMPRSS2 axis additional pathways can be altered in a lung and kidney that might modify survival and tissue injury/repair. Genes from these key pathways could be involved in lung-kidney cross-talk in COVID-19 patient. We have identified 9 genes, expression of which was significantly changed during experimental PMV and AKI; theses changes were common to both organs during injurious response. Out of common 9 genes 3 were previously described as AKI-related genes (Lcn2, Socs3, and Inhbb); other six genes were novel (Mt2, Maff, Junb, Hmgcs2, Tnfrsf12a and Ch25h)