ACE inhibitors, angiotensin receptor blockers and endothelial injury in COVID‐19

Background COVID‐19 is caused by the coronavirus SARS‐CoV‐2, which uses angiotensin‐converting enzyme 2 (ACE‐2) as a receptor for cellular entry. It is theorized that ACE inhibitors (ACE‐Is) or angiotensin receptor blockers (ARBs) may increase vulnerability to SARS‐CoV‐2 by upregulating ACE‐2 expres...

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Published in:	Journal of internal medicine Vol. 289; no. 5; pp. 688 - 699
Main Authors:	Tetlow, S., Segiet‐Swiecicka, A., O’Sullivan, R., O’Halloran, S., Kalb, K., Brathwaite‐Shirley, C., Alger, L., Ankuli, A., Baig, M.S., Catmur, F., Chan, T., Dudley, D., Fisher, J., Iqbal, M.U., Puczynska, J., Wilkins, R., Bygate, R., Roberts, P.
Format:	Journal Article
Language:	English
Published:	England Blackwell Publishing Ltd 01-05-2021 John Wiley and Sons Inc
Subjects:	ACE inhibitors Acute Kidney Injury - diagnosis Acute Kidney Injury - etiology Age Factors Aged Angiotensin Receptor Antagonists - therapeutic use Angiotensin-converting enzyme inhibitors Angiotensin-Converting Enzyme Inhibitors - therapeutic use Cardiology Comorbidity Coronaviruses COVID-19 COVID-19 - diagnosis COVID-19 - mortality COVID-19 - physiopathology critical care Diabetes mellitus Diabetes Mellitus - epidemiology endothelial function Epidermal growth factor receptors Female Glomerular Filtration Rate Hospital Mortality Humans Hypertension - drug therapy Hypertension - epidemiology Immunosuppression infectious disease Inhibitors Kidney diseases Kidneys Male Mortality Original Outcome and Process Assessment, Health Care Pandemics Receptors renal failure Renal Insufficiency, Chronic - epidemiology Renal Insufficiency, Chronic - therapy Risk Risk Adjustment - methods SARS-CoV-2 - isolation & purification Severe acute respiratory syndrome Severe acute respiratory syndrome coronavirus 2 Thromboembolism Thrombosis Thrombosis - diagnosis Thrombosis - etiology United Kingdom - epidemiology Viral diseases Withholding Treatment - standards Withholding Treatment - statistics & numerical data United Kingdom endothelial function critical care renal failure thrombosis infectious disease ACE inhibitors
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Summary:	Background COVID‐19 is caused by the coronavirus SARS‐CoV‐2, which uses angiotensin‐converting enzyme 2 (ACE‐2) as a receptor for cellular entry. It is theorized that ACE inhibitors (ACE‐Is) or angiotensin receptor blockers (ARBs) may increase vulnerability to SARS‐CoV‐2 by upregulating ACE‐2 expression, but ACE‐I/ARB discontinuation is associated with clinical deterioration. Objective To determine whether ACE‐I and ARB use is associated with acute kidney injury (AKI), macrovascular thrombosis and in‐hospital mortality. Methods A retrospective, single‐centre study of 558 hospital inpatients with confirmed COVID‐19 admitted from 1 March to 30 April 2020, followed up until 24 May 2020. AKI and macrovascular thrombosis were primary end‐points, and in‐hospital mortality was a secondary end‐point. Results AKI occurred in 126 (23.1%) patients, 34 (6.1%) developed macrovascular thrombi, and 200 (35.9%) died. Overlap propensity score‐weighted analysis showed no significant effect of ACE‐I/ARB use on the risk of occurrence of the specified end‐points. On exploratory analysis, severe chronic kidney disease (CKD) increases odds of macrovascular thrombi (OR: 8.237, 95% CI: 1.689–40.181, P = 0.009). The risk of AKI increased with advancing age (OR: 1.028, 95% CI: 1.011–1.044, P = 0.001) and diabetes (OR: 1.675, 95% CI: 1.065–2.633, P = 0.025). Immunosuppression was associated with lower risk of AKI (OR: 0.160, 95% CI: 0.029–0.886, P = 0.036). Advancing age, dependence on care, male gender and eGFR < 60 mL min−1/1.73 m2 increased odds of in‐hospital mortality. Conclusion We did not identify an association between ACE‐I/ARB use and AKI, macrovascular thrombi or mortality. This supports the recommendations of the European and American Societies of Cardiology that ACE‐Is and ARBs should not be discontinued during the COVID‐19 pandemic.
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ISSN:	0954-6820 1365-2796
DOI:	10.1111/joim.13202