Iron Replacement With Ferric Citrate Hydrate

Because iron deficiency anemia (IDA) increases levels of C-terminal fibroblast growth factor 23 (cFGF23) and platelet count (PLT), both associated with cardiovascular events, Kyoko Ito and others hypothesized that iron replacement with ferric citrate hydrate (FC) would decrease cFGF23 levels and PLT in patients with IDA. To test this theory, they conducted a randomized, open-label, multicenter, 24-week clinical trial.

They randomized patients with nondialysis-dependent chronic kidney disease (CKD) and non-CKD complicated by IDA (8.0 ≤ hemoglobin <11.0 g/dL; serum ferritin <50 ng/mL [CKD] and <12 ng/mL [non-CKD]) 1:1 to FC-low (500 mg: elemental iron approximately 120 mg/day) or FC-high (1000 mg: elemental iron approximately 240 mg/day). Treatment was discontinued if adequate iron replacement had been achieved after 8 weeks.

The researchers assigned 73 patients to FC-low (CKD, n=21; non-CKD, n=15) and FC-high (CKD, n=21; non-CKD, n=16). FC increased serum ferritin and transferrin saturation, did not change intact cFGF23 or serum phosphorus, and decreased cFGF23 regardless of CKD status. In the FC-high group, median changes in cFGF23 from baseline to week 8 were −66.00 RU/mL in CKD and −649.50 RU/mL in non-CKD. In the FC-low group, the median changes were −58.00 RU/mL in CKD and −725.00 RU/mL in non-CKD. By week 8, FC treatment regularized PLT in all patients with high PLT at baseline (>35.2 × 10⁴/µL; FC-low: 1 CKD, 8 non-CKD; FC-high: 3 CKD, 8 non-CKD).

The results showed that iron replacement with FC decreased elevated cFGF23 levels and normalized elevated PLT in patients with IDA regardless of CKD status.

Source: Clinical and Experimental Nephrology