РОЛЬ ФАКТОРА РОСТА ФИБРОБЛАСТОВ-23 В ПАТОГЕНЕЗЕ НАРУШЕНИЙ ОБМЕНА ФОСФОРА ПРИ НЕФРОПАТИЯХ У ДЕТЕЙ

INTRODUCTION: Fibroblast growth factor-23 (FGF-23) is a phosphaturic hormone, synthesized by osteocytes and involved in the pathogenesis of several hypophosphatemic diseases. THE AIM OF STUDYwas to evaluate influence of intact (iFGF-23) on mineral metabolism in children with different nephropathies. PATIENTS AND METHODS: 87 children, age from 7 months to 17 years 10 months were included in the study. Level of intact FGF-23 was measured (with ELISA) in children with hypophosphatemic rickets (n=15), Fanconi syndrome (n=9), chronic kidney disease stage 3-5 (n=35), steroid osteoporosis (n=10) and in children without nephropathies (n=18). Routine biochemistry markers of phosphate metabolism were measured in children with kidney diseases. RESULTS: FGF-23 level in comparison group was 22,92 pg/ml (5,91-54,37), 5 children were excluded because of undetectable level (<5 pg/ml). All children with kidney diseases had significantly elevated FGF-23 level (in comparison with healthy children): in children with hypophosphatemic rickets FGF-23 level was 73,11 pg/ml (40,08-125,71), p<0,01, in Fanconi syndrome patients - 141,56 pg/ml (34,27-302,64), p<0,01, CKD 3-5 stage patients - 613,71 pg/ml (20,15-6230,77), p<0,01, osteoporosis patients - 106,65 pg/ml (61,64-147,74), p<0,01. Correlation between FGF-23 level and eGFR (using Schwartz formula) in CKD 3-5 stage was found, r= -0,678, p<0,01. Children with Fanconi syndrome on phosphate and vitamin D supplementation had elevated FGF-23 level and we found the strong correlation between FGF-23 level and serum phosphate level (r=0,843, p<0,05) despite of hypophosphatemia. CONCLUSIONS: Our results suggest that FGF-23 is involved in pathogenesis of mineral disorders in different nephropathies. Besides, FGF-23 is rising with the progression of CKD, reaching maximum level in 5-th stage of CKD in pediatric patients as in adult ones.