Cardioprotective Effects of Paricalcitol Alone and in Combination With FGF23 Receptor Inhibition in Chronic Renal Failure: Experimental and Clinical Studies
Author(s) -
Brian Czaya,
Wacharee Seeherunvong,
Saurav Singh,
Christopher Yanucil,
Phillip Ruiz,
Yasmir Quiroz,
Alexander Grabner,
Chryso Katsoufis,
Sethuraman Swaminathan,
Carolyn Abitbol,
Bernardo RodríguezIturbe,
Christian Faul,
Michael Freundlich
Publication year - 2018
Publication title -
american journal of hypertension
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.009
H-Index - 136
eISSN - 1941-7225
pISSN - 0895-7061
DOI - 10.1093/ajh/hpy154
Subject(s) - medicine , calcineurin , endocrinology , paricalcitol , nfat , kidney disease , secondary hyperparathyroidism , transplantation , parathyroid hormone , calcium
In uremic animals, vitamin D receptor (VDR) agonists like paricalcitol (Pc) attenuate cardiac hypertrophy, but this effect has not been replicated consistently in humans with chronic kidney disease. Elevated fibroblast growth factor 23 (FGF23) levels cause cardiac hypertrophy with activation of the myocardial calcineurin/nuclear factor of activated T cell (NFAT) axis and may antagonize the cardioprotective effects of VDR agonist therapy. We hypothesized that the effectiveness of Pc may depend on the prevailing circulating levels of FGF23 and could be potentiated by the combined administration of a pan-FGF23 receptor (FGFR) blocker agent (PD173074).
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