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Alexander Kutz, Anna Conen, Claudia Gregoriano, Sebastian Haubitz, Daniel Koch, Oliver Domenig, Luca Bernasconi, Beat Mueller, and Philipp Schuetz

Objective

While evidence on the interface between severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection and the renin-angiotensin-aldosterone-system (RAAS) is accumulating, clinical data on RAAS peptide alteration among coronavirus disease-19 (COVID-19) patients is missing.

Design and methods

In this exploratory study, we prospectively included adult patients (aged ≥ 18 years) admitted between February 26 and April 30, 2020 to a tertiary care hospital in Switzerland. We assessed the association of an underlying SARS-CoV-2 infection and equilibrium serum levels of RAAS peptides in hospitalized COVID-19 patients 1:1 propensity-score matched with patients suffering from SARS-CoV-2-negative respiratory infections. Subgroup analyses involved stratification for taking RAAS inhibitors.

Results

COVID-19 patients had about 50% lower equilibrium serum RAAS peptide levels as compared with matched controls (angiotensin I: 31.6 vs 66.8 pmol/L, −52.7% (95%CI: −68.5% to −36.9%); angiotensin II: 37.7 vs 92.5 pmol/L, −59.2% (95%CI: −72.1% to −46.3%); angiotensin (1–5): 3.3 vs 6.6 pmol/L, −49.7% (95%CI: −59.2% to −40.2%); angiotensin (1–7): 4.8 vs 7.6 pmol/L, −64.9% (95%CI: −84.5% to −45.3%)). While the plasma renin activity was lower in COVID-19 patients (88.6 vs 207.9 pmol/L, −58.5% (95%CI: −71.4% to −45.6%)), there was no difference of angiotensin-converting enzyme (ACE) and ACE2 plasma activity between the groups. Subgroup analyses revealed a pronounced RAAS peptide profile depression in COVID-19 patients among those not on RAAS inhibitors.

Conclusions

As compared with SARS-CoV-2-negative patients, we found a downregulated RAAS in presence of a SARS-CoV-2 infection. Whether the lower levels of the protective angiotensin (1–5) and (1–7) are linked to adverse outcomes in COVID-19 warrants further investigation.