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?:abstract
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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 up-regulating 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-center study of 558 hospital inpatients with confirmed COVID-19 admitted from 1st March - 30th April 2020, followed up until 24th May 2020 AKI and macrovascular thrombosis were primary endpoints, in-hospital mortality was a secondary endpoint RESULTS: AKI occurred in 126 (23 1%) patients, 34 (6 1%) developed macrovascular thrombi, 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 endpoints 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 2 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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