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C-Terminal Fibroblast Growth Factor-23 Levels in Non-Nutritional Hypophosphatemic Rickets
Joyita Bharati1, Divya Bhatia1, Priyanka Khandelwal1
1Division of Nephrology, Department of Pediatrics, All India Institute of Medical Sciences, Ansari Nagar, New Delhi, 110029, India.
Insights
Blood Fibroblast Growth Factor-23 (FGF23) levels did not distinguish classic hypophosphatemic rickets from other hypophosphatemic conditions in children. FGF23 concentrations were similar across various rickets types, indicating limited diagnostic utility.
Area of Science:
- Pediatric Endocrinology
- Nephrology
- Metabolic Bone Disease
Background:
- Fibroblast growth factor-23 (FGF23) plays a crucial role in phosphate and vitamin D metabolism.
- Distinguishing classic hypophosphatemic rickets from other causes of hypophosphatemia is clinically important for appropriate management.
Purpose of the Study:
- To investigate whether serum FGF23 levels can differentiate classic hypophosphatemic rickets from other non-nutritional rickets with hypophosphatemia in children.
- To assess the correlation of FGF23 levels with biochemical parameters in these conditions.
Main Methods:
- A cohort of 42 children with non-nutritional rickets and hypophosphatemia were clinically classified into five groups: distal renal tubular acidosis (RTA), Fanconi syndrome, classic hypophosphatemic rickets, vitamin D dependent rickets, and Dent disease.
- Serum FGF23 concentrations were measured using a C-terminal ELISA.
- Correlations between FGF23 levels and phosphate, tubular maximum for phosphate, calcium, 25-hydroxyvitamin D, creatinine, and parathormone were analyzed.
Main Results:
- Median serum FGF23 concentrations were similar across all studied groups (P=0.24).
- FGF23 levels did not show significant correlations with phosphate, tubular maximum for phosphate, calcium, 25-hydroxyvitamin D, creatinine, or parathormone.
- Patients with distal RTA exhibited transient proximal tubular dysfunction that resolved with alkali supplementation.
Conclusions:
- Serum FGF23 levels are not a reliable biomarker for differentiating classic hypophosphatemic rickets from other causes of hypophosphatemic rickets in children.
- The diagnostic utility of FGF23 in the context of various hypophosphatemic rickets is limited.
Abstract:
Fibroblast growth factor-23 (FGF23) is central to phosphate homeostasis. The author examined if blood levels of FGF23 allow discrimination of classic hypophosphatemic rickets from other causes of non-nutritional rickets with hypophosphatemia. Forty-two children (median age: 102 mo) with non-nutritional rickets and hypophosphatemia were clinically classified as having distal renal tubular acidosis (RTA, n = 12), Fanconi syndrome (n = 8), classic hypophosphatemic rickets (n = 11), vitamin D dependent rickets (n = 7) and Dent disease (n = 4). Median blood FGF23 (measured by C-terminal ELISA) concentrations were similar in all groups (P = 0.24). These levels did not correlate with phosphate, tubular maximum for phosphate, calcium, 25-hydroxyvitamin D, creatinine, and parathormone levels. Patients with distal RTA showed variable degree of proximal tubular dysfunction that resolved following alkali supplements. Blood FGF23 levels did not satisfactorily differentiate classic hypophosphatemic rickets from other causes of hypophosphatemic rickets.
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