Interestingly, in this study declining sKL protein levels in the heart in combination with elevated FGF23 production correlated with cardiac hypertrophy, indicating that a reduction in sKL’s inhibitory actions toward FGF23’s pro-hypertrophic effects might contribute to uremic cardiomyopathy (185), thereby supporting the hypothesis that sKL can act as a decoy receptor for FGF23, as discussed above. Here, FGF23 is linked to cardiac hypertrophy.