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Review
. 2020 Jul;34(7):e13991.
doi: 10.1111/ctr.13991. Epub 2020 Jun 15.

What solid organ transplant healthcare providers should know about renin-angiotensin-aldosterone system inhibitors and COVID-19

Affiliations
Review

What solid organ transplant healthcare providers should know about renin-angiotensin-aldosterone system inhibitors and COVID-19

Sunnie Y Wong et al. Clin Transplant. 2020 Jul.

Abstract

The data on the outcomes of solid organ transplant recipients who have contracted coronavirus disease 2019 (COVID-19) are still emerging. Kidney transplant recipients are commonly prescribed renin-angiotensin-aldosterone system (AAS) inhibitors given the prevalence of hypertension, diabetes, and cardiovascular disease. As the angiotensin-converting enzyme 2 (ACE2) facilitates the entry of coronaviruses into target cells, there have been hypotheses that preexisting use of renin-angiotensin-aldosterone system (RAAS) inhibitors may increase the risk of developing severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection. Given the common use of RAAS inhibitors among solid organ transplant recipients, we sought to review the RAAS cascade, the mechanism of SARS-CoV-2 entry, and pertinent data related to the effect of RAAS inhibitors on ACE2 to guide management of solid organ transplant recipients during the COVID-19 pandemic. At present, there is no clear evidence to support the discontinuation of RAAS inhibitors in solid organ transplant recipients during the COVID-19 pandemic.

Keywords: ACE2 receptor; COVID-19; renin-angiotensin-aldosterone inhibitors; solid organ transplant.

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Conflict of interest statement

We have no conflict of interest.

Figures

FIGURE 1
FIGURE 1
A, Classic RAAS: Renin cleaves angiotensinogen to form angiotensin I, which is then converted to angiotensin II by ACE. B, Angiotensin I can be converted to angiotensin 1‐9, and Angiotensin II to Angiotensin 1‐7, by ACE2, a homologue of ACE. This ACE 2‐dependent pathway counterbalances the classic pathway
FIGURE 2
FIGURE 2
(LEFT) Membrane‐bound ACE2 is required to facilitate cellular entry of SARS‐CoV‐2. (RIGHT) When cleaved by ADAM17, ACE2 is released extracellularly. The soluble form of ACE2 is shown to prevent SAR‐CoV‐2 entry in preclinical experiments

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