Immunity in maintenance immunosuppression with and without cyclosporine in long-term kidney transplant recipients

2000 ◽  
Vol 32 (7) ◽  
pp. 1768-1772
Author(s):  
M Yamashita ◽  
A Aikawa
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.


2018 ◽  
Vol 19 (5) ◽  
pp. 1444-1451 ◽  
Author(s):  
Hege K. Pihlstrøm ◽  
Geir Mjøen ◽  
Sören Mucha ◽  
Andre Franke ◽  
Alan Jardine ◽  
...  

2014 ◽  
Vol 97 (9) ◽  
pp. 925-933 ◽  
Author(s):  
Jeffrey J. Gaynor ◽  
Gaetano Ciancio ◽  
Giselle Guerra ◽  
Junichiro Sageshima ◽  
Lois Hanson ◽  
...  

2012 ◽  
Vol 94 (10S) ◽  
pp. 362
Author(s):  
N. Goto ◽  
Y. Matsuda ◽  
M. Takada ◽  
T. Yamamoto ◽  
M. Tsujita ◽  
...  

2019 ◽  
Vol 103 (8) ◽  
pp. 1705-1713 ◽  
Author(s):  
Tracey Ying ◽  
Germaine Wong ◽  
Wai H. Lim ◽  
Philip Clayton ◽  
John Kanellis ◽  
...  

2002 ◽  
Vol 87 (02) ◽  
pp. 194-198 ◽  
Author(s):  
Torsten Slowinski ◽  
Ingeborg Hauser ◽  
Birgit Vetter ◽  
Lutz Fritsche ◽  
Daniela Bachert ◽  
...  

SummaryWe analysed whether the factor V Leiden mutation – the most common hereditary predisposing factor for venous thrombosis – is associated with early and long-term graft dysfunction after kidney transplantation in 394 Caucasian kidney transplant recipients. The presence of factor V Leiden mutation was identified by allele specific PCR. The prevalence of the factor V Leiden mutation was compared to 32216 unselected neonates. The prevalence of the factor V Leiden mutation (GA genotype) was similar in 394 kidney transplant recipients and 32216 neonates. The frequency of known factors predicting long-term graft function were similar in patients with the GA genotype and with the normal factor V gene (GG genotype). The GA genotype was associated with the occurrence of no primary graft function (risk: 2.87; 95% confidence interval: 1.01-8.26; p < 0.05), the number of dialysis after transplantation in patients with no primary graft function until graft function (7.5 ± 2.06 dialysis in GA patients; 4.2 ± 0.36 dialyses in GG patients; p < 0.05), and the risk for at least one acute rejection episode (risk: 3.83; 95% confidence interval: 1.38-10.59; p < 0.02). The slope of 1/creatinine per year was significantly lower in patients with the GA genotype (GA patients: – 0.0204 ± 0.008 dl/mg per year; GG patients: 0.0104 ± 0.004 dl/mg per year; p < 0.02). The annual enhancement of the daily protein excretion rate was elevated in patients with the GA genotype (GA patients: 38.5 ± 16.6 mg/24 h per year; GG patients: 4.9 ± 4.4 mg/24 h per year; p < 0.02). Our study showed that the factor V Leiden mutation is associated with the occurrence of delayed graft function, acute rejection episodes and chronic graft dysfunction after kidney transplantation.


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