FGF23 and uremia: All previously reported animal models developing LVH in the presence of elevated circulating Fgf23 levels due to experimental uremia, genetic deletion of klotho, high phosphate diet, or injection of recombinant FGF23 protein display a variety of systemic changes that are all proven contributors to cardiac injury, making it difficult to elucidate the causative role of FGF23 for LVH in these studies (Faul et al., 2011; Andrukhova et al., 2014; Grabner et al., 2015; Hu et al., 2015; Yang et al., 2015; Leifheit-Nestler et al., 2017).