Background: The discovery of fibroblast growth factor 23 (FGF23) provides a new conceptual framework that improves our understanding of the pathogenesis of post-transplant bone disease. Excess FGF23 is produced in the early post-transplant period; levels return to normal in the months following transplant. However, the importance of FGF23 levels in the long term is unknown. Methods: We performed a cross-sectional observational study of 279 maintenance kidney recipients with chronic kidney disease (CKD) stages 1-4 and stable allograft function who had received their transplant at least 12 months previously. Results: FGF23, parathyroid hormone (PTH), and phosphorus values were higher in more advanced stages, while serum 1,25(OH)2 vitamin D levels and phosphate reabsorption rate were lower (table 1).A significant inverse correlation was found between eGFR and FGF23 (r=-0.417;p< 0.001), PTH (r=-0.422;p< 0.001), serum phosphate levels (r=-0.254;p< 0.001), serum magnesium (r=-0.136; p=0.023), and fractional excretion of magnesium (r=-0.483; p< 0.001). Multivariate analysis showed that increased time on corticosteroids, PTH, serum phosphate, proteinuria, decreased serum calcitriol, and estimated glomerular filtration rate were associated with high FGF23 levels. In contrast with pretransplant patients and first year post-transplant patients, higher FGF23 values were not correlated with increased phosphate excretion. Conclusions: FGF23 concentrations are increased in maintenance kidney recipients, even during the early stages of CKD. Decreasing time on corticosteroids, PTH, and serum phosphate could help reduce FGF23 levels. Further research will show whether lowering FGF23 levels improves outcome in kidney recipients.