Effect of Sucroferric Oxyhydroxide on Fibroblast Growth Factor 23 Levels in Hemodialysis Patients

Otsuki, Tomoyasu; Utsunomiya, Kei; Moriuchi, Masari; Horikoshi, Shu; Okamura, Mitsu; Suzuki, Hiroko; Okamura, Makiyo; Maruyama, Noriaki; Shibahara, Nami; Abe, Masanori

doi:10.1159/000490903

Cited by 9 publications

(6 citation statements)

References 32 publications

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“…The phosphate-lowering effect of sucroferric oxyhydroxide was maintained over 1 year of follow-up, and no iron overload was observed. In hemodialysis patients, sucroferric oxyhydroxide may lead to an increase in serum iron parameters, albeit to a much lesser extent than what is observed with ferric citrate 100, 101, 102…”

Section: Dietary Phosphate Restrictionmentioning

confidence: 90%

Strategies for Phosphate Control in Patients With CKD

Barreto

Massy

et al. 2019

Kidney International Reports

102

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Hyperphosphatemia is a common complication in patients with chronic kidney disease (CKD), particularly in those requiring renal replacement therapy. The importance of controlling serum phosphate has long been recognized based on observational epidemiological studies that linked increased phosphate levels to adverse outcomes and higher mortality risk. Experimental data further supported the role of phosphate in the development of bone and cardiovascular diseases. Recent advances in our understanding of the mechanisms involved in phosphate homeostasis have made it clear that the serum phosphate concentration depends on a complex interplay among the kidneys, intestinal tract, and bone, and is tightly regulated by a complex endocrine system. Moreover, the source of dietary phosphate and the use of phosphate-based additives in industrialized foods are additional factors that are of particular importance in CKD. Not surprisingly, the management of hyperphosphatemia is difficult, and, despite a multifaceted approach, it remains unsuccessful in many patients. An additional issue is the fact that the supposedly beneficial effect of phosphate lowering on hard clinical outcomes in interventional trials is a matter of ongoing debate. In this review, we discuss currently available treatment approaches for controlling hyperphosphatemia, including dietary phosphate restriction, reduction of intestinal phosphate absorption, phosphate removal by dialysis, and management of renal osteodystrophy, with particular focus on practical challenges and limitations, and on potential benefits and harms.

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Section: Dietary Phosphate Restrictionmentioning

confidence: 90%

Strategies for Phosphate Control in Patients With CKD

Barreto

Massy

et al. 2019

Kidney International Reports

102

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“…Several studies have confirmed that iron-containing phosphate binders lower FGF23 in HD patients and that the ability of the agents to lower FGF23 levels may be independent of the effect of a decrease in phosphate [16][17][18][19]. In the present study, the changes in the levels of TSAT and phosphate were serially higher and lower in the oral iron group than those in the iv iron and non-iron treatment groups, respectively, and a high TSAT was an independent factor for decreased intact FGF23 levels.…”

Section: Discussionmentioning

confidence: 95%

Differential Impacts of Intravenous Iron Administration and Iron-Containing Phosphate Binders on Serum Intact Fibroblast Growth Factor 23 Levels

Honda

Tanaka²,

Michihata

et al. 2019

Blood Purif

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Aims: This study assessed the impact of iron administration on serum fibroblast growth factor 23 (FGF23) levels. Methods: Of 123 hemodialysis (HD) patients treated with erythropoiesis-stimulating agents, 22 received once-weekly intravenous iron and 17 received daily oral iron with iron-containing phosphate binders. Intact FGF23 and biomarkers of iron metabolism were measured from blood samples drawn before each HD session, at baseline and on days 3, 5, 7, and 14. Results: Phosphate levels did not differ among the 3 groups during the 14-day period. Ferritin levels were significantly increased in both iron treatment groups compared with the non-iron treatment group, but changes in transferrin saturation levels were similar in the intravenous iron and non-iron groups. However, intact FGF23 levels were continuously higher in the intravenous iron group than those in the other groups. Conclusion: Intravenous iron administration may influence intact FGF23 levels in HD patients independently of phosphate and iron metabolism.

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“…To further investigate the effect of different phosphate binders on reducing serum intact FGF23 levels in patients with CKD, we performed a subgroup analysis (Figure 4). 6 studies used iron-based phosphate binders to treat patients with CKD (33,36,37,39,41,42), while 7 studies used noniron-based phosphate binders to treat patients with CKD (27,34,35,38,40,43,44). There was a significant statistical difference, indicating that the effect of ferric citrate on decreasing serum intact FGF23 levels was better than noiron phosphate binders (P<0.05).…”

Section: Subgroup Analysismentioning

confidence: 99%

“…One was whether the patient's dietary phosphorus intake was restricted. There were 4 studies restricted patient's dietary phosphate intake (37,38,41,42), while 9 studies did not restrict patient's dietary phosphate intake during the treatment (27,(33)(34)(35)(36)39,40,43,44). The other was whether patients performed hemodialysis.…”

Section: Meta-regressionmentioning

confidence: 99%