In conclusion, the present study showed that the effect of HP intake on bone metabolism and aortic calcification did not depend on estrogen status; in contrast, HP intake synergistically induced nephrocalcinosis in the presence of estrogenic action on the bone, and FGF23 was involved in nephrocalcinosis induced by HP intake partially through FGFR1 signaling. The gene discussed is FGFR1; the disease is nephrocalcinosis.