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. Author manuscript; available in PMC: 2015 Jul 1.
Published in final edited form as: Arterioscler Thromb Vasc Biol. 2014 May 22;34(7):1399–1411. doi: 10.1161/ATVBAHA.114.303508

Figure 7. Proposed model of LVH in CKD.

Figure 7

Increased serum concentration of S100/calgranulins in mice with CKD promotes systemic inflammation in a RAGE-dependent manner, and this is associated with cartilagenous metaplasia and calcification of the valve annulus. Importantly, systemic inflammation in vivo (and in cultured cardiac fibroblasts upon treatment with cytokines), up regulates endogenous FGF23 in cardiac fibroblasts, which may act in a paracrine manner to promote LVH and diastolic dysfunction. Elevated serum FGF23 has been previously associated with LVH and recombinant FGF23 was shown to directly cause hypertrophy of cardiac myocytes in vitro and in vivo (ref. 24).