Iron Deficiency Linked With Elevated FGF-23 in Pediatric CKD
Iron deficiency may contribute to the relationship between proteinuria and excess FGF-23, researchers suggested.
SAN DIEGO—Iron deficiency may promote elevated levels of fibroblast growth factor 23 (FGF-23) in pediatric chronic kidney disease (CKD) patients, investigators revealed at Kidney Week 2015.
For the CKiD Study, Farah N. Ali, MD, MS of Northwestern University Feinberg School of Medicine in Chicago, Ill., and colleagues assessed laboratory results from 551 pediatric CKD patients. On average, the estimated glomerular filtration rate (eGFR) was 53 mL/min/1.73 m2 and transferrin saturation (TSAT) was 26%. The median level of ferritin was 46 ng/mL; urine protein/creatinine 0.31 mg/mg; and c-terminal FGF-23 114 RU/mL.
The investigators observed that cFGF-23 was inversely related to ferritin and eGFR and directly related to C-reactive protein, proteinuria, and phosphate. The investigators also looked at the degree of proteinuria (low or high) and found that total iron binding capacity was lower and cFGF-23 was higher in the high proteinuria group.
Results showed that cFGF-23 levels were significantly elevated in patients with the lowest ferritin levels, especially in early stages of CKD. Multivariable analysis revealed that only lower eGFR, glomerular disease, higher phosphate, and lower ferritin independently predicted higher cFGF-23 levels. When ferritin was introduced to the model, the relationship between proteinuria and cFGF-23 lessened.
“FGF-23, a powerful marker of mortality in CKD, may have a metabolic pathway related to iron,” Dr. Ali told Renal & Urology News. “This is important because iron deficiency is a modifiable disease state. Potentially we could find a way to alter the production of FGF-23 in early CKD by using iron, possibly leading to beneficial effects on outcomes.”