Effect of ferric citrate on serum phosphate and fibroblast growth factor 23 among patients with nondialysis-dependent chronic kidney disease: path analyses
| Autor: | Geoffrey A. Block, Pablo E. Pergola, John F. Neylan, Steven Fishbane, Robin D. LeWinter, Julian G. Martins, Katrin Uhlig, Glenn M. Chertow |
|---|---|
| Jazyk: | angličtina |
| Rok vydání: | 2018 |
| Předmět: |
Fibroblast growth factor 23
Male medicine.medical_specialty Anemia Population 030232 urology & nephrology iron-deficiency anemia Enzyme-Linked Immunosorbent Assay 030204 cardiovascular system & hematology Ferric Compounds Phosphates 03 medical and health sciences 0302 clinical medicine Double-Blind Method FGF23 Renal Dialysis Internal medicine medicine Humans nondialysis-dependent chronic kidney disease Renal Insufficiency Chronic education serum phosphate Aged Transplantation education.field_of_study Anemia Iron-Deficiency Transferrin saturation business.industry medicine.disease ferric citrate Fibroblast Growth Factors stomatognathic diseases Fibroblast Growth Factor-23 Endocrinology Basic Research Iron-deficiency anemia Nephrology Ferric Female Hemoglobin ORIGINAL ARTICLES business Biomarkers Kidney disease medicine.drug Follow-Up Studies |
| Zdroj: | Nephrology Dialysis Transplantation |
| ISSN: | 1460-2385 0931-0509 |
| Popis: | Background Among patients with nondialysis-dependent chronic kidney disease (NDD-CKD) and iron-deficiency anemia (IDA), ferric citrate increases hemoglobin and iron parameters and reduces serum phosphate and fibroblast growth factor 23 (FGF23), a key phosphate-regulating hormone. We conducted post hoc analyses of a phase 3 trial to explore associations between iron replacement, serum phosphate changes and FGF23 regulation. Methods We employed multivariable regression and longitudinal mixed-effects models to identify and confirm, respectively, whether baseline demographic and laboratory variables were associated with ferric citrate-induced changes in serum phosphate or FGF23 concentrations. We employed path analyses to determine whether changes in FGF23 concentrations were mediated via changes in serum phosphate and/or transferrin saturation (TSAT). Results We analyzed a total of 117 and 115 ferric citrate-treated and placebo-treated patients, respectively. At 16 weeks, ferric citrate significantly reduced serum phosphate versus placebo (P = 0.006) only among patients with elevated baseline serum phosphate (≥4.5 mg/dL) and did not reduce serum phosphate among patients with baseline serum phosphate within the population reference range. Ferric citrate reduced intact FGF23 and C-terminal FGF23 partially via changes in TSAT (for C-terminal FGF23) and serum phosphate (for intact FGF23) and partially via unknown/unmeasured mechanisms. Conclusions Ferric citrate reduced serum FGF23 concentrations (partially via effects on serum phosphate and iron balance) and did not reduce serum phosphate among patients with baseline serum phosphate concentrations within the population reference range. |
| Databáze: | OpenAIRE |
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