ACE-Inhibitors, Angiotensin Receptor Blockers and Endothelia
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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.

This study aimed to determine whether ACE-I and ARB use is associated with Acute Kidney Injury (AKI), macrovascular thrombosis, and in-hospital mortality.

A retrospective, single-center study of 558 hospital inpatients with confirmed COVID-19 was carried out. AKI and macrovascular thrombosis were primary endpoints, in-hospital mortality was a secondary endpoint.

-- 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.

-- The risk of AKI increased with advancing age and diabetes. Immunosuppression was associated with lower risk of AKI.

-- Advancing age, dependence on care, male gender and eGFR less than 60ml/min/1.73m2 increased odds of in-hospital mortality.

Conclusively, researchers 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.