Skip to main page content
U.S. flag

An official website of the United States government

Dot gov

The .gov means it’s official.
Federal government websites often end in .gov or .mil. Before sharing sensitive information, make sure you’re on a federal government site.

Https

The site is secure.
The https:// ensures that you are connecting to the official website and that any information you provide is encrypted and transmitted securely.

Access keys NCBI Homepage MyNCBI Homepage Main Content Main Navigation
Randomized Controlled Trial
. 2019 Jun 20;9(1):8877.
doi: 10.1038/s41598-019-45335-4.

Randomised clinical trial of ferric citrate hydrate on anaemia management in haemodialysis patients with hyperphosphataemia: ASTRIO study

Keitaro Yokoyama  1 , Masafumi Fukagawa  2 , Takashi Akiba  3 , Masaaki Nakayama  4   5 , Kyoko Ito  6 , Koji Hanaki  7 , Myles Wolf  8 , Hideki Hirakata  9
Affiliations
Randomized Controlled Trial

Randomised clinical trial of ferric citrate hydrate on anaemia management in haemodialysis patients with hyperphosphataemia: ASTRIO study

Keitaro Yokoyama et al. Sci Rep. .

Abstract

Ferric citrate hydrate (FC) is an iron-based phosphate binder approved for hyperphosphataemia in patients with chronic kidney disease. We conducted a randomised controlled trial to evaluate the effects of FC on anaemia management in haemodialysis patients with hyperphosphataemia. We 1:1 randomised 93 patients who were undergoing haemodialysis and being treated with non-iron-based phosphate binders and erythropoiesis-stimulating agents (ESA) to receive 24 weeks of FC or to continue their non-iron-based phosphate binders (control) in a multicentre, open-label, parallel-design. Phosphate level was controlled within target range (3.5-6.0 mg/dL). The primary endpoint was change in ESA dose from baseline to end of treatment. Secondary endpoints were changes in red blood cell, iron and mineral, and bone-related parameters. Compared with control, FC reduced ESA dose [mean change (SD), -1211.8 (3609.5) versus +1195 (6662.8) IU/week; P = 0.03] without significant differences in haemoglobin. FC decreased red blood cell distribution width (RDW) compared with control. While there were no changes in serum phosphate, FC reduced C-terminal fibroblast growth factor (FGF) 23 compared with control. The incidence of adverse events did not differ significantly between groups. Despite unchanged phosphate and haemoglobin levels, FC reduced ESA dose, RDW, and C-terminal FGF23 compared with control.

PubMed Disclaimer

Conflict of interest statement

K.Y., M.F., T.A. and H.H. received consulting fees from Torii Pharmaceutical Co. Ltd. and Japan Tobacco, Inc. M.N. received research funding and consulting fees from Torii Pharmaceutical Co. Ltd. and Japan Tobacco, Inc. M.W. received consulting fees from Torii Pharmaceutical Co. Ltd. and Keryx Biopharmaceuticals, Inc. K.I. is an employee of Torii Pharmaceutical Co. Ltd. and K.H. is an employee of Japan Tobacco Inc. The study was conducted by the funding from Torii Pharmaceutical Co., Ltd. (Tokyo, Japan) and Japan Tobacco Inc. (Tokyo, Japan).

Figures

Figure 1
Figure 1
Study design.
Figure 2
Figure 2
Consolidated standards of the reporting trial.
Figure 3
Figure 3
FC reduced ESA dose during the study. The proportions of patients receiving an ESA dose greater than 5,000 IU/week decreased in the FC group compared with the control [FC: baseline, n = 19, 41.3%; week 24, n = 8, 23.5%; control: baseline, n = 18, 40.0%; week 24, n = 24, 58.5%].
Figure 4
Figure 4
Scatter plot of serum ferritin and hepcidin in the FC group. The actual measured values obtained at baseline, weeks 12 and 24 were subjected to regression analyses with serum ferritin as the objective variable and hepcidin as the explanatory variable to calculate Pearson’s correlation coefficients and P-values. Baseline (n = 46): y = 19.99 + 1.45x; r = 0.85 (P < 0.001). Week 12 (n = 34): y = 90.05 + 0.56x; r = 0.48 (P < 0.004). Week 24 (n = 33): y = 100.81 + 0.64x; r = 0.54 (P < 0.001).
See this image and copyright information in PMC

References

    1. Masakane I, et al. An overview of regular dialysis treatment in Japan (as of 31 December 2013) Ther. Apher. Dial. 2015;19:540–574. doi: 10.1111/1744-9987.12378. - DOI - PubMed
    1. Waheed AA, Pedraza F, Lenz O, Isakova T. Phosphate control in end-stage renal disease: barriers and opportunities. Nephrol. Dial. Transplant. 2013;28:2961–2968. doi: 10.1093/ndt/gft244. - DOI - PMC - PubMed
    1. Block GA, et al. Mineral metabolism, mortality, and morbidity in maintenance hemodialysis. J. Am. Soc. Nephrol. 2004;15:2208–2218. doi: 10.1097/01.ASN.0000133041.27682.A2. - DOI - PubMed
    1. Noordzij M, et al. Progression of aortic calcification is associated with disorders of mineral metabolism and mortality in chronic dialysis patients. Nephrol. Dial. Transplant. 2011;26:1662–1669. doi: 10.1093/ndt/gfq582. - DOI - PubMed
    1. Silverberg DS, Wexler D, Iaina A. The importance of anemia and its correction in the management of severe congestive heart failure. Eur. J. Heart. Fail. 2002;4:681–686. doi: 10.1016/S1388-9842(02)00115-0. - DOI - PubMed

Publication types