Pathophysiological mechanisms of calcineurin inhibitor-induced nephrotoxicity and arterial hypertension

Result code in IS VaVaI

<a href="https://www.isvavai.cz/riv?ss=detail&h=RIV%2F00023001%3A_____%2F17%3A00075868" target="_blank" >RIV/00023001:_____/17:00075868 - isvavai.cz</a>

Result on the web

<a href="http://www.biomed.cas.cz/physiolres/pdf/66/66_167.pdf" target="_blank" >http://www.biomed.cas.cz/physiolres/pdf/66/66_167.pdf</a>

DOI - Digital Object Identifier

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Result language

angličtina

Original language name

Pathophysiological mechanisms of calcineurin inhibitor-induced nephrotoxicity and arterial hypertension

Original language description

Solid organ transplantation is an established treatment modality in patients with end-stage organ damage in cases where other therapeutic options fail. The long-term outcomes of solid organ transplant recipients have improved considerably since the introduction of the first calcineurin inhibitor (CNI) - cyclosporine. In 1984, the potent immunosuppressive properties of another CNI, tacrolimus, were discovered. The immunosuppressive effects of CNIs result from the inhibition of interleukin-2 synthesis and reduced proliferation of T cells due to calcineurin blockade. The considerable side effects that are associated with CNIs therapy include arterial hypertension and nephrotoxicity. The focus of this article was to review the available literature on the pathophysiological mechanisms of CNIs that induce chronic nephrotoxicity and arterial hypertension. CNIs lead to activation of the major vasoconstriction systems, such as the reninangiotensin and endothelin systems, and increase sympathetic nerve activity. On the other hand, CNIs are known to inhibit NO synthesis and NO-mediated vasodilation and to increase free radical formation. Altogether, these processes cause endothelial dysfunction and contribute to the impairment of organ function. A better insight into the mechanisms underlying CNI nephrotoxicity could assist in developing more targeted therapies of arterial hypertension or preventing CNI nephrotoxicity in organ transplant recipients, including heart transplantation.

Czech name

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Czech description

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Type

J_imp - Article in a specialist periodical, which is included in the Web of Science database

CEP classification

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OECD FORD branch

30201 - Cardiac and Cardiovascular systems

Project

<a href="/en/project/NV15-25396A" target="_blank" >NV15-25396A: Central and peripheral modulation of vascular tone and sodium excretion: the role of brain and kidney in pathophysiology of hypertension</a><br>

Continuities

P - Projekt vyzkumu a vyvoje financovany z verejnych zdroju (s odkazem do CEP)<br>I - Institucionalni podpora na dlouhodoby koncepcni rozvoj vyzkumne organizace

Publication year

2017

Confidentiality

S - Úplné a pravdivé údaje o projektu nepodléhají ochraně podle zvláštních právních předpisů

Name of the periodical

Physiological research

ISSN

0862-8408

e-ISSN

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Volume of the periodical

66

Issue of the periodical within the volume

2

Country of publishing house

CZ - CZECH REPUBLIC

Number of pages

14

Pages from-to

167-180

UT code for WoS article

000404258800001

EID of the result in the Scopus database

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