The Role of Fibroblast Growth Factor 23 as a Marker of Early Renal Impairment in Children with Type 1 Diabetes Mellitus

Abstract

Background: Diabetic nephropathy (DN), a leading complication of type 1 diabetes mellitus (T1DM) in children, remains a major contributor to end-stage renal disease. Emerging evidence suggests that tubular injury, rather than glomerular damage alone, may initiate renal dysfunction. Fibroblast Growth Factor 23 (FGF23), a regulator of phosphate metabolism, has been implicated in early kidney injury. This study aimed to assess FGF23 as a potential early biomarker of renal impairment in children with T1DM.Methods: This cross-sectional study included 50 children with T1DM (duration >5 years). Clinical assessments and laboratory investigations including HbA1C, eGFR, albumin/creatinine ratio (ACR), and serum FGF23 levels were conducted. Early renal impairment was defined as ACR ≥30 mg/g. Results: Early renal impairment was identified in 44% of patients. Children with renal impairment had significantly higher FGF23 levels (76 ± 10 vs. 51 ± 11 pg/mL, P < 0.001), higher HbA1C (10.4 ± 2 vs. 9 ± 1.5%, P = 0.009), and lower eGFR (78.9 ± 11.7 vs. 94.1 ± 21.6 mL/min/1.73m², P = 0.003). FGF23 positively correlated with phosphorus, creatinine, and ACR, and inversely with eGFR. ROC analysis showed excellent diagnostic accuracy for FGF23 (AUC = 0.955; cutoff >67 pg/mL; sensitivity: 86.4%, specificity: 96.4%). Multivariate analysis revealed FGF23 (OR = 1.414, P = 0.02) and HbA1C (OR = 5.529, P = 0.046) as independent predictors of early renal impairment. Conclusion: Elevated serum FGF23 is significantly associated with early renal impairment in T1DM children and may serve as a promising early biomarker to guide timely intervention.