Renin-Angiotensin-Aldosterone System peptide profiles in patients with COVID-19

in European Journal of Endocrinology
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  • 1 A Kutz, University Department of Medicine, Kantonsspital Aarau, Aarau, Switzerland
  • 2 A Conen, University Department of Medicine, Kantonsspital Aarau, Aarau, Switzerland
  • 3 C Gregoriano, University Department of Medicine, Kantonsspital Aarau AG, Aarau, Switzerland
  • 4 S Haubitz, University Department of Medicine, Kantonsspital Aarau, Aarau, Switzerland
  • 5 D Koch, Division of Endocrinology, Diabetes, and Metabolism; University Department of Medicine, Kantonsspital Aarau AG, Aarau, Switzerland
  • 6 O Domening, Attoquant Diagnostics GmbH, Campus Vienna Biocenter, Wien, Austria
  • 7 L Bernasconi, Institute of Laboratory Medicine, Kantonsspital Aarau AG, Aarau, Switzerland
  • 8 B Mueller, University Department of Medicine, Kantonsspital Aarau, Aarau, Switzerland
  • 9 P Schuetz, University Department of Medicine, Kantonsspital Aarau, Aarau, Switzerland

Correspondence: Alexander Kutz, Email: kutz.alexander@gmail.com
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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. 66.8pmol/l, -52.7% [95%CI -68.5% to -36.9%]; angiotensin II: 37.7 vs. 92.5pmol/l, -59.2% [95%CI -72.1% to -46.3%]; angiotensin (1-5): 3.3 vs. 6.6pmol/l, -49.7% [95%CI -59.2% to -40.2%]; angiotensin (1-7): 4.8 vs. 7.6pmol/l, -64.9% [95%CI -84.5% to -45.3%]). While the plasma renin activity (PRA-S) was lower in COVID-19 patients (88.6 vs. 207.9pmol/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.

 

     European Society of Endocrinology

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