HYPERRENINISM - A COMMON PHENOMENON IN HOSPITALIZED COVID-19 PATIENTS

Abstract

Objective: Since the beginning of the worldwide pandemic the interaction of SARS-CoV2 on renin-angiotensin-aldosterone system is discussed intensively. Since ACE-2 was identified as the cellular receptor of SARS-CoV-2, the debate started with the question, whether treatment with ACE-inhibitors (ACE-I) and angiotensin receptor blockers (ARB) should be discontinued during the pandemic. In contrast, current studies investigate a potential benefit by ACE-I, ARB and mineralocorticoid receptor antagonists. However, data on renin and aldosterone concentrations in patients with COVID-19 are sparse. Design and method: We performed a cross-sectional study in 52 patients hospitalized for moderate COVID-19 (peripheral ward, no intensive care) assessing renin and aldosterone after admission. Blood pressure, comorbidities and medication were documented. Results: 50% of the patients had increased renin concentrations with a median of 57.35ng/ml (IQR 34.3 - 80.1). 13.5% had decreased concentrations. 36.5% had a renin concentration within normal range. Median renin concentration in the overall study population was 24ng/ml (IQR 6.8 - 60.28). Despite the high percentage of patients with hyperreninism, only 13.5% showed increased levels of aldosterone 366pg/ml (IQR 268-384). There were no cases of primary hyperaldosteronism. Median aldosterone concentration was 81.5pg/ml (IQR 34.3-80.1) in the overall population. Those patients with secondary hyperaldosteronism revealed hypokalemia in 0%, metabolic alkalosis in 0%, and hypertension in 0%. Median renin concentration did not significantly differ in subjects with and without ACE-I or ARB 17ng/ml (5,6-69.6) vs. 24.4ng/ml (5.5-57.3), p = 0.91. Conclusions: Hyperreninism is a frequent phenomenon and occurs in every second patient hospitalized for COVID 19. This finding could not be explained by volume depletion, hypotension, or use of ACE-I/ARB. Both the reason for this finding and the infrequent translation into secondary hyperaldosteronism will have to be investigated in future studies.