Background
Activation of the vasopressin system plays a key role for the maintenance of osmotic, cardiovascular and stress hormone homeostasis during disease. We investigated levels of copeptin, the C-terminal segment of the vasopressin prohormone, that mirrors the production rate of vasopressin in patients infected with severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2).
Methods
We measured levels of copeptin on admission and after 3/4, 5/6 and 7/8 days in 74 consecutive hospitalized adult COVID-19 patients and compared its prognostic accuracy to that of patients with community-acquired pneumonia (n=876) and acute or chronic bronchitis (n=371) from a previous study by means of logistic regression analysis. The primary endpoint was all-cause 30-day mortality.
Results
Median admission copeptin levels in COVID-19 patients were almost 4-fold higher in non-survivors compared to survivors (49.4 pmol/L (IQR 24.9-68.9 pmol/L) vs. 13.5 pmol/L (IQR 7.0-26.7 pmol/L) resulting in an age and gender-adjusted odds ratio of 7.0 (95%CI 1.2 to 40.3), p<0.03 for mortality. Higher copeptin levels in non-survivors persisted during the short-term follow-up. Compared to the control group patients with acute/chronic bronchitis and pneumonia, COVID-19 patients did not have higher admission copeptin levels.
Conclusions
A pronounced activation of the vasopressin system in COVID-19 patients is associated with an adverse clinical course in COVID-19 patients. This finding, however, is not unique to COVID-19 but similar to other types of respiratory infections. .