High levels of fibroblast growth factor 23 (FGF23) have been associated with increased cardiovascular disease and mortality risk in patients with chronic kidney disease (CKD). In a recent paper published in International Urology and Nephrology, investigators reported that certain treatment strategies may reduce FGF23, a phosphaturic hormone, better than others.
Paweena Susantitaphong, MD, and colleagues from Chulalongkorn University in Bangkok, Thailand, conducted a systematic review of 36 randomized controlled trials and 5 prospective studies on FGF23 involving 7590 patients with CKD. According to their meta-analysis, noncalcium-based phosphate binders (eg, sevelamer, lanthanum, and iron-based binders), iron supplements, and calcimimetics significantly reduce FGF23 levels by a standardized mean difference (SMD) of 1.18, 1.44, and 1.25, respectively.
With respect to therapies that remove FGF23, a middle-molecule uremic toxin, Dr Susantitaphong’s team found that hemodiafiltration, hemoperfusion, and preservation of residual renal function significantly reduced FGF23 levels by a SMD of 1.65, 1.39, and 0.52, respectively, in patients receiving dialysis.
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Conversely, the investigators found that dietary phosphate restriction to less than 800 mg/d, parathyroidectomy, and high flux dialysis did not significantly reduce FGF23 levels. The number of included studies and duration of treatment possibly affected these outcomes, the investigators noted.
Whether lowering FGF23 improves clinical outcomes warrants further study, according to the study authors. They also suggested future studies on novel therapies, including FGF23 antibodies and FGF23 receptor blockers, in this population.
Reference
Takkavatakarn K, Wuttiputhanun T, Phannajit J, Praditpornsilpa K, Eiam‑Ong S, Susantitaphong P. Effectiveness of fibroblast growth factor 23 lowering modalities in chronic kidney disease: a systematic review and meta‑analysis. Published online April 2, 2021. Int Urol Nephrol. doi:10.1007/s11255-021-02848-0
