Key result
SARS-CoV-2 infection was associated with ~50% lower equilibrium serum RAAS peptide levels (e.g., angiotensin I: 31.6 vs 66.8 pmol/L) compared with SARS-CoV-2-negative respiratory infections.
Why the study?
While evidence on the interface between SARS-CoV-2 infection and the RAAS was accumulating, clinical data on RAAS peptide alteration in COVID-19 patients was missing.
Does SARS-CoV-2 infection alter equilibrium serum levels of RAAS peptides compared to SARS-CoV-2-negative respiratory infections in hospitalized adults?
Population
Hospitalized adult patients aged ≥ 18 years at a tertiary care hospital in Switzerland
Comparison
COVID-19 patients vs 1:1 propensity-score matched SARS-CoV-2-negative respiratory infection controls
Design
Prospective exploratory propensity-score matched study
Authors
Loading...
SARS-CoV-2 may suppress RAAS peptides versus other infections; observational data leaves open causal and prognostic implications.
Observational
No
Does SARS-CoV-2 infection alter equilibrium serum levels of RAAS peptides compared to SARS-CoV-2-negative respiratory infections in hospitalized adults?
Effect estimate: -52.7% (95% CI -68.5% to -36.9%)
Absolute Event Rate: 31.6% vs 66.8%
Hospitalized COVID-19 patients exhibit a downregulated renin-angiotensin-aldosterone system peptide profile compared to patients with non-COVID-19 respiratory infections.
Kutz et al. (2021) conducted an observational in COVID-19. SARS-CoV-2 infection vs. SARS-CoV-2-negative respiratory infections was evaluated on Equilibrium serum angiotensin I levels (pmol/L) (-52.7%, 95% CI -68.5% to -36.9%). SARS-CoV-2 infection was associated with ~50% lower equilibrium serum RAAS peptide levels (e.g., angiotensin I: 31.6 vs 66.8 pmol/L) compared with SARS-CoV-2-negative respiratory infections.
Synapse has enriched 5 closely related papers on similar clinical questions. Consider them for comparative context: