They found out that some genes related to ACE in comparison to genes related to ACE2 are more 'expressed' in Covid patients than normally and they conclude that that must have resulted in too much bradykinine. Hmm - that strikes me as kind of roundabout - why they couldn't just measure bradykinine levels directly? Is that too hard?<p>"Here, we perform a new analysis on gene expression data from cells in bronchoalveolar lavage fluid (BALF) from COVID-19 patients that were used to sequence the virus. Comparison with BALF from controls identifies a critical imbalance in RAS represented by decreased expression of ACE in combination with increases in ACE2, renin, angiotensin, key RAS receptors, kinogen and many kallikrein enzymes that activate it, and both bradykinin receptors. This very atypical pattern of the RAS is predicted to elevate bradykinin levels in multiple tissues and systems that will likely cause increases in vascular dilation, vascular permeability and hypotension."