Background. Hypokalemia is a common electrolyte complication among hospitalized patients with pneumonia caused by a new coronavirus SARS-CoV-2. Hyperactivation of the renin-angiotensin-aldosterone system (RAAS) is suggested as a possible cause of hypokalemia in patients with COVID-19. Objective. To investigate the RAAS activity in COVID-19 patients with and without hypokalemia and its possible association with treatment outcomes. Design and methods. The cross-sectional cohort study included 172 patients with COVID-19 pneumonia. Potassium, aldosterone and venous renin were measured in 77 patients. The differences in the levels of acute phase proteins, the degree of lung damage and the severity of COVID-19 were compared between patients with and without hypokalemia. Results. Hypokalemia was found in 19 of 77 patients (25%): the median potassium level in hypokalemia and eukalemia group was 3,1 [2,8-3,3] and 4,1 [3,9-4,5] mmol/L, respectively (p = 0,001). Plasma aldosterone and renin levels in patients with and without hypokalemia did not differ significantly: aldosterone 76,0 [57,7-121,5] and 70,9 [26,3-113,8] pg/ml (p = 0,23), renin 17,0 [8,5-47,2] and 11,0 [6,5-38,1] pg/ml (p = 0,35), respectively. Differences in the degree of lung tissue damage, acute phase proteins, severity of COVID-19, length of hospitalization and mortality in patients with and without identified electrolyte disturbances were also not significant. Conclusions. Our results showed that there were no laboratory signs of RAAS hyperactivation in COVID-19 patients with registered hypokalemia. Identification of the cause and clinical significance of hypokalemia among patients with COVID-19 needs to be specified. © 2021 All-Russian Public Organization Antihypertensive League. All rights reserved.
Hypokalemia and the renin-angiotensin-aldosterone system activity in COVID-19 patients