tetano
Editor, Senior Moderator
J Intern Med
. 2020 Nov 18.
doi: 10.1111/joim.13202. Online ahead of print.
ACE-Inhibitors, Angiotensin Receptor Blockers and Endothelial Injury in COVID-19
Simon Tetlow[SUP] 1 [/SUP], Agnieszka Segiet-Swiecicka[SUP] 2 3 [/SUP], Rebecca O'Sullivan[SUP] 4 [/SUP], Sinead O'Halloran[SUP] 4 [/SUP], Kelli Kalb[SUP] 4 [/SUP], Charlotte Brathwaite-Shirley[SUP] 4 [/SUP], Laura Alger[SUP] 4 [/SUP], Akshay Ankuli[SUP] 4 [/SUP], Mirza Shaheer Baig[SUP] 4 [/SUP], Fergus Catmur[SUP] 4 [/SUP], Torbert Chan[SUP] 4 [/SUP], Declan Dudley[SUP] 4 [/SUP], Joshua Fisher[SUP] 4 [/SUP], Muhammad Usman Iqbal[SUP] 4 [/SUP], Joanna Puczynska[SUP] 4 [/SUP], Ryan Wilkins[SUP] 4 [/SUP], Rachael Bygate[SUP] 5 [/SUP], Peter Roberts[SUP] 4 [/SUP]
Affiliations
Abstract
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 1[SUP]st[/SUP] March - 30[SUP]th[/SUP] April 2020, followed up until 24[SUP]th[/SUP] 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 <60ml/min/1.73m[SUP]2[/SUP] 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.
Keywords: ACE-Inhibitors; Critical Care; Endothelial Function; Infectious Disease; Renal Failure; Thrombosis.
. 2020 Nov 18.
doi: 10.1111/joim.13202. Online ahead of print.
ACE-Inhibitors, Angiotensin Receptor Blockers and Endothelial Injury in COVID-19
Simon Tetlow[SUP] 1 [/SUP], Agnieszka Segiet-Swiecicka[SUP] 2 3 [/SUP], Rebecca O'Sullivan[SUP] 4 [/SUP], Sinead O'Halloran[SUP] 4 [/SUP], Kelli Kalb[SUP] 4 [/SUP], Charlotte Brathwaite-Shirley[SUP] 4 [/SUP], Laura Alger[SUP] 4 [/SUP], Akshay Ankuli[SUP] 4 [/SUP], Mirza Shaheer Baig[SUP] 4 [/SUP], Fergus Catmur[SUP] 4 [/SUP], Torbert Chan[SUP] 4 [/SUP], Declan Dudley[SUP] 4 [/SUP], Joshua Fisher[SUP] 4 [/SUP], Muhammad Usman Iqbal[SUP] 4 [/SUP], Joanna Puczynska[SUP] 4 [/SUP], Ryan Wilkins[SUP] 4 [/SUP], Rachael Bygate[SUP] 5 [/SUP], Peter Roberts[SUP] 4 [/SUP]
Affiliations
- PMID: 33210357
- DOI: 10.1111/joim.13202
Abstract
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 1[SUP]st[/SUP] March - 30[SUP]th[/SUP] April 2020, followed up until 24[SUP]th[/SUP] 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 <60ml/min/1.73m[SUP]2[/SUP] 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.
Keywords: ACE-Inhibitors; Critical Care; Endothelial Function; Infectious Disease; Renal Failure; Thrombosis.