Abstract: SA-PO419

Oral Iron Therapy and Serum Hepcidin in Children with CKD

Session Information

Category: Chronic Kidney Disease (Non-Dialysis)

  • 302 CKD: Estimating Equations, Incidence, Prevalence, Special Populations

Authors

  • Amini, Ameneh, Weill Cornell College of Medicine, New York, New York, United States
  • Gautam, Richa, Weill Cornell College of Medicine, New York, New York, United States
  • Perelstein, Eduardo M., Weill Cornell College of Medicine, New York, New York, United States
  • Rivella, Stefano, Children's Hospital of Philadelphia, Philadelphia, Pennsylvania, United States
  • Choi, Mary E., Weill Cornell College of Medicine, New York, New York, United States
  • Kumar, Juhi, Weill Cornell College of Medicine, New York, New York, United States
  • Akchurin, Oleh M., Weill Cornell College of Medicine, New York, New York, United States
Background

Hepatic peptide hepcidin, a major regulator of iron homeostasis, is up-regulated in adults and children with chronic kidney disease (CKD). Hepcidin blockade ameliorates renal anemia in experimental CKD. Iron and inflammation contribute to hepcidin over-production in animal models and in adult patients with CKD. However, the relationship between oral iron therapy and hepcidin in children with CKD has not been characterized.

Methods

Cross-sectional single center study. Serum hepcidin was measured by ELISA (Intrinsic Lifesciences, USA). Clinical data were abstracted from medical records of children with stages 2-5 CKD. Platelet-to-lymphocyte ratio (PLR) was used as a marker of inflammation. Glomerular filtration rate (GFR) was estimated using bedside Schwartz formula. Normally distributed data are shown as mean±SD. T-test and linear regression were used for data analysis.

Results

Hepcidin was measured in 36 childern ( 60% males, median age 12.5). Hepcidin strongly correlated with serum ferritin (r=0.64, p<0.005) and modestly with total iron binding capacity (TIBC; r=-0.43, p=0.02), and GFR (r=-0.34, p=0.04). There was a trend toward correlation between hepcidin and hemoglobin (r=-0.29, nondirectional p=0.09, directional p=0.04). No significant correlation was observed between serum hepcidin and PLR (r=0.1). Oral iron therapy was prescribed to 14 children (Fe+ group) and not prescribed to 22 (Fe-). GFR was 34.6 and 47.4 mL/min/1.73m2 in the Fe+ and Fe- groups, respectively (p=0.03). Fe+ group had lower hemoglobin compared to Fe- group (11.7±1.5 vs. 13.0±2.0, p=0.04), but similar serum iron, ferritin, TIBC, and transferrin saturation. Serum hepcidin was higher in the Fe+ group than in Fe- group (94.6±41 ng/mL vs. 44±78, p=0.015). This difference remained significant after adjusting for age, sex, CKD etiology (glomerular vs. non-glomerular) and PLR (adjusted p=0.017), and was attenuated after additional adjustment for GFR (adjusted p=0.05).

Conclusion

In this pediatric CKD cohort, serum hepcidin was associated with iron therapy status, independently of PLR. Additional analyses of inflammatory markers in this cohort are ongoing. Further investigations of the impact of iron-mediated hepcidin elevation on clinically relevant outcomes in childern with CKD are warranted.