We investigated whether the phosphate (Pi) load in the circulation causes renal damage in non-CKD women. This cross-sectional study included 1,094 non-CKD Japanese women. Fibroblast growth factor (FGF)-23 as a parameter for the Pi load, bone alkaline phosphatase (BAP) as a bone metabolic marker, and the urinary albumin-to-creatinine ratio (UACR) as an early marker for renal damage were measured. Postmenopausal women exhibited significantly higher levels of serum Pi, FGF-23, BAP, and UACR and significantly lower eGFR than premenopausal women. In postmenopausal women, a multiple regression analysis confirmed a correlation between serum BAP and log UACR. In premenopausal women, although serum FGF-23 did not correlate with log UACR, a multiple regression analysis revealed that FGF-23 correlated with log UACR. Based on the i ncrease observed in BAP and its close relationship with log UACR in postmenopausal women, the release of Pi from bone may be linked to the systemic circulation of Pi, which has the potential to induce renal and vascular damage. Therefore, serum FGF-23 may be a useful marker for renal and vascular damage in premenopausal women; however, it currently remains unclear whether FGF-23 by itself or as a surrogate marker for the Pi load induces damage in the kidney and/or vasculature.