scholarly journals Improvement in renal function in kidney transplant recipients switched from cyclosporine or tacrolimus to belatacept: 2-year results from the long-term extension of a phase II study

2012 ◽  
Vol 25 (10) ◽  
pp. 1059-1064 ◽  
Author(s):  
Josep Grinyo ◽  
Josefina Alberu ◽  
Fabiana L. C. Contieri ◽  
Roberto C. Manfro ◽  
Guillermo Mondragon ◽  
...  
2010 ◽  
Vol 55 (4) ◽  
pp. B75
Author(s):  
Lissa Levin ◽  
Gregory Malat ◽  
Mohit Gupta ◽  
Muhammad Saeed ◽  
Snehankita Kulkarni ◽  
...  

2017 ◽  
Vol 17 (12) ◽  
pp. 3219-3227 ◽  
Author(s):  
F. Vincenti ◽  
G. Blancho ◽  
A. Durrbach ◽  
G. Grannas ◽  
J. Grinyó ◽  
...  

Diabetes ◽  
1988 ◽  
Vol 37 (9) ◽  
pp. 1247-1252 ◽  
Author(s):  
J. A. Van der Vliet ◽  
X. Navarro ◽  
W. R. Kennedy ◽  
F. C. Goetz ◽  
J. J. Barbosa ◽  
...  

2021 ◽  
Vol 46 (2) ◽  
pp. 245-249
Author(s):  
Monika Cahova ◽  
Martin Kveton ◽  
Vojtech Petr ◽  
David Funda ◽  
Helena Dankova ◽  
...  

<b><i>Background:</i></b> Preclinical studies suggested that pharmacological inhibition of the renin-angiotensin-aldosterone system (RAAS) by ACE inhibitors (ACEis) or angiotensin II receptor blockers (ARBs) may increase local angiotensin-converting enzyme 2 (<i>ACE2</i>) expression. <b><i>Methods:</i></b> In this study, we evaluated the effect of ACEi or ARB treatment on expression of <i>ACE2</i>, <i>ACE</i>, and <i>AGTR1</i> in 3-month protocol kidney allograft biopsies of stable patients using RT-qPCR (<i>n</i> = 48). Protein ACE2 expression was assessed using immunohistochemistry from paraffin sections. <b><i>Results:</i></b> The therapy with RAAS blockers was not associated with increased <i>ACE2, ACE</i>, or <i>ATGR1</i> expression in kidney allografts and also ACE2 protein immunohistochemistry did not reveal differences among groups. <b><i>Conclusions:</i></b> ACEis or ARBs in kidney transplant recipients do not affect local ACE2 expression. This observation supports long-term RAAS treatment in kidney transplant recipients, despite acute complications such as COVID-19 where ACE2 serves as the entry protein for infection.


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