(1) Background: Cirrhotic patients have an increased risk for severe
COVID-19. We investigated the renin-angiotensin-aldosterone system (RAS), parameters of endothelial dysfunction,
inflammation, and coagulation/fibrinolysis in cirrhotic patients and in
COVID-19 patients. (2) Methods: 127 prospectively characterized cirrhotic patients (CIRR), along with nine patients with mild
COVID-19 (mild-COVID), 11 patients with
COVID-19 acute respiratory distress syndrome (ARDS; ARDS-COVID), and 10 healthy subjects (HS) were included in the study.
Portal hypertension (PH) in cirrhotic patients was characterized by hepatic venous pressure gradient (HVPG). (3) Results: With increased
liver disease severity (Child-Pugh stage A vs. B vs. C) and compared to HS, CIRR patients exhibited higher RAS activity (
angiotensin-converting enzyme (ACE),
renin,
aldosterone), endothelial dysfunction (
von Willebrand-factor (VWF)
antigen),
inflammation (
C-reactive protein (CRP),
interleukin-6 (IL-6)), and a disturbed coagulation/fibrinolysis profile (
prothrombin fragment F1,2,
D-dimer,
plasminogen activity,
antiplasmin activity). Increased RAS activity (
renin), endothelial dysfunction (vWF), coagulation parameters (
D-dimer,
prothrombin fragment F1,2) and
inflammation (CRP, IL-6) were significantly altered in COVID patients and followed similar trends from mild-COVID to ARDS-COVID. In CIRR patients, ACE activity was linked to
IL-6 (ρ = 0.26; p = 0.003), independently correlated with VWF
antigen (aB: 0.10; p = 0.001), and was inversely associated with
prothrombin fragment F1,2 (aB: -0.03; p = 0.023) and
antiplasmin activity (aB: -0.58; p = 0.006), after adjusting for
liver disease severity. (4) Conclusions: The considerable upregulation of the RAS in Child-Pugh B/C
cirrhosis is linked to systemic
inflammation, endothelial dysfunction, and abnormal coagulation profile. The
cirrhosis-associated abnormalities of ACE,
IL-6, VWF
antigen, and
antiplasmin parallel those observed in severe
COVID-19.