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. 2019 Nov 6;11(11):647. doi: 10.3390/toxins11110647

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© 2019 by the authors.

Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license (http://creativecommons.org/licenses/by/4.0/).

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Cardiovascular pathomechanisms of elevated FGF23 and hyperphosphatemia in chronic kidney disease (CKD). The phosphate excretion attenuates with declining kidney function. Resulting FGF23 elevation counteracts the phosphate retention by downregulating NaPi-2a/c in the kidney, but also directly promotes LVH via FGFR4–calcineruin–NFAT signaling. FGF23 induces hypertension by activation of the RAAS and NCC expression. Hyperphosphatemia stimulates the osteochondrogenic differentiation and release of Ca/P loaded vesicles in VSMCs via Pit-1, and thereby induces VC. Phosphate-induced vascular calcification (VC) together with activation of the RAAS and SNA contribute to the development of hypertension. eGFR, estimated glomerulus filtration rate; NaPi-2a/c, type IIa/c sodium-dependent phosphate transporter; FGFR4, fibroblast growth factor receptor 4; NFAT, nuclear factor of activated T-cells; RAAS, renin-angiotensin-aldosterone system; NCC, Na⁺Cl⁻ co-transporter; SNA, sympathetic nerve system; VC, vascular calcification.