Article Type

Original Study


Objective The objective of this study was to evaluate the possible role of fibroblast growth factor 23 (FGF23) in the occurrence of left ventricular hypertrophy and vascular calcification in predialysis chronic kidney disease (CKD) patients. Background FGF23 is a suggested risk factor for poor outcome of CKD. This raises the possibility that FGF23 is a hormone that controls calcium–phosphorus metabolism and is a real risk factor for cardiovascular mortality and morbidity in predialysis CKD patients. Materials and methods Thirty predialysis CKD patients with estimated glomerular filtration rate (90≥eGFR>15 ml/min/1.73 m2) by the modification of diet in renal diseases formula were included in this study. Patients were recruited from the Internal Medicine Department, Menoufia University (Egypt). Our controls were 10 individuals with preserved kidney function of more than 90 ml/min/1.73 m2 with normal BUN and creatinine matched by age and sex. Routine and specific investigations (serum FGF23 measurement using ELISA immunoassay, serum intact parathyroid hormone, conventional echocardiography, and lateral abdominal aortic radiograph for calcification) were performed. Results The mean log FGF23 level in CKD patients was 2.3±0.6 Ru/ml and was significantly higher than that of control participants, 1.7±0.1 Ru/ml (P<0.001). There was a significant difference between CKD2–3 stage and CKD4 stage in the FGF23 (P<0.05) level but not in serum phosphorus (P>0.05). Left ventricular mass index was correlated positively with log FGF23 (r=0.44, P<0.05) and negatively with eGFR (r=−0.4, P<0.05). Abdominal aortic calcification was correlated positively with age (r=0.55, P<0.001), but had no correlation with FGF23 (r=0.36, P>0.05). Conclusion FGF23 could be an early risk factor for the occurrence of left ventricular hypertrophy even before an increase in serum phosphorus in predialysis CKD patients.