Fibroblast growth factor 23(FGF23) is the most important
biomarker and pathogenic factor in
Chronic Kidney Disease-Mineral and Bone Disorder (
CKD-MBD). In the moderate and severe stages of
chronic renal failure, abnormally elevated circulating FGF23 can lead to some complications, including myocardial
hypertrophy, which is positively correlated with all-cause mortality. However, the circulating FGF23 level of different
hemodialysis modalities, the underlying essential regulatory factors, and potential clinical benefits remain to be elucidated. In this retrospective cohort study, 90 in-center nocturnal
hemodialysis (INHD) and 90 matched conventional
hemodialysis (CHD) patients were enrolled. The complete blood count, intact FGF23(iFGF23),
calcium,
phosphorus, PTH, and other biochemical and echocardiographic parameters of INHD and CHD patients were collected and analyzed at 1-year follow-up. The all-cause mortality was recorded during the 7-year follow-up. Furthermore, the regulatory factors of iFGF23 and its association with echocardiographic parameters and mortality were investigated by multivariate regression. The levels of iFGF23 and serum
phosphate in patients undergoing INHD were significantly lower than those in patients undergoing CHD. The left ventricular volume index (LVMI) in patients with INHD was significantly attenuated and positively correlated with the drop of serum iFGF23. The INHD group had reduced all-cause mortality compared to the CHD group. Multivariate analysis showed that iFGF23 was positively correlated with serum
calcium, serum
phosphorus, and
calcium-phosphate product. The
calcium-phosphate product is an independent determining factor of serum iFGF23. Compared with the CHD group, the INHD group presented with a significantly reduced circulating iFGF23 level, which was closely associated with attenuation of
left ventricular hypertrophy, but INHD reduced all-cause mortality in an FGF23 independent manner.