Oral Low-Dose Ferric Citrate Is a Useful Iron Source for Hyperphosphatemic Hemodialysis Patients: A Case Series

2016 ◽  
Vol 43 (1-3) ◽  
pp. 97-100 ◽  
Author(s):  
Masayuki Tanemoto ◽  
Yu Ishimoto ◽  
Hisako Saito
Keyword(s):  
Phosphate Binder ◽  
Low Dose ◽  
Transferrin Saturation ◽  
Case Series ◽  
Ferric Citrate ◽  
Phosphate Binders ◽  
Iron Stores ◽  
Median Serum ◽  
Iron Deficient ◽  
Iron Parameters

Background: Randomized trials have demonstrated that a phosphate binder ferric citrate (FeC) increases iron parameters in comparison with other phosphate binders, but the doses for FeC to improve iron stores safely have not been clarified. Methods: We examined changes of iron parameters and blood hemoglobin (Hb) in 7 iron-deficient hemodialysis (HD) patients taking FeC 750 mg/day as a phosphate binder. Results: The median serum transferrin saturation and ferritin increased from 13% (interquartile range (IQR) 7-18) to 28% (IQR 22-31; p = 0.010) and from 17 ng/ml (IQR 11-60) to 106 ng/ml (IQR 58-176; p = 0.015) by 2 and 3 months respectively. With the persistence of these levels thereafter, the FeC administration reduced the usage of erythropoiesis-stimulating agents while maintaining adequate blood Hb levels. Conclusion: Oral FeC 750 mg/day improves iron stores without inducing iron overload in hyperphosphatemic HD patients.

P1411THE EFFICACY AND SAFETY OF THE SUCROFFERRIC OXYHYDXIDE IN HEMODIALYSIS PATIENTS : RESULTS OF A PROSPECTIVE RANDOMIZED CONTROLLED TRIAL

2020 ◽  
Vol 35 (Supplement_3) ◽  
Author(s):  
Evgeny Shutov ◽  
Galina Kotlyarova ◽  
Ksenia Lysenko ◽  
Galina Ryabinskaya ◽  
Sergey Lashutin
Keyword(s):  
Randomized Controlled Trial ◽  
Phosphate Binder ◽  
Controlled Trial ◽  
Transferrin Saturation ◽  
Serum Phosphate ◽  
Phosphate Binders ◽  
Randomized Controlled ◽  
Prospective Randomized Controlled Trial ◽  
Sevelamer Carbonate ◽  
Fgf 23

Abstract Background and Aims The treatment of hyperphosphatemia is the main goal in the treatment of mineral and bone disorders in patients with CKD. However, the results of the correction of hyperphosphatemia remain unsatisfactory. This is due to the absence of effective and safe medicines. In our prospective randomized controlled trial were evaluated the effects of a 16-week treatment with new phosphate binder - sucroferric oxyhydroxide and a sevelamer carbonate (“sevelamer”) on CKD-MBD parameters in patients on hemodialysis with hyperphosphatemia. Method After a 2-4-week washout period from previous phosphate binders, 50 stable patients with hyperphosphatemia (P > 5.5 mg / dl) were randomized at a 1: 1 ratio to receive sucroferric oxyhydroxide (n = 25) or sevelamer (n = 25) for treatment up to 16 weeks. In all patients were evaluated levels of P, Ca, PTH, ferritin, transferrin saturation, Hb, FGF-23, soluble Klotho, CRP - monthly. The dose of both medications was adjusted according to serum phosphate. Results Phosphate binder therapy of sucroferric oxyhydroxide was associated with a significant decrease in serum phosphate from 6.8 ± 1.5 to 5.27 ± 0.99 mg/dl (p <0.01); however, treatment with sevelamer did not decrease in the level of P: 6.32 ± 1.5 vs 6.35 ± 1.9 mgl/dl. The number of tablets was lower in the sucroferric oxyhydroxide group (mean ± SD 2.0 ± 1.5 tablets / day) compared with sevelamer (mean ± SD 6.1 ± 3.2 tablets / day). The average intact fibroblast growth factor-23 (FGF-23), PTH, transferrin saturation and ferritin did not significantly change in both groups. Klotho changed only in patients received sucroferric oxyhydroxide, an increase of 25% (р < 0.05) and we also noted in this group an increase in Hb level from 105.6 ± 15.7 to 111.9 ± 22.3 g/l (p <0.05) by the end of the study, simultaneously level of CRP significantly decreased (P < 0.01) by 50% . During the study, 6 patients in the group with sucroferric oxyhydroxide and 5 in the sevelamer group dropped out due to dyspeptic symptoms. Conclusion Sucroferric oxyhydroxide is a new effective phosphate binder with a comparable safety profile to a sevelamer. Treatment with this drug can significantly increase the level of Hb, and Klotho and reduce level of inflammation.

scholarly journals Effect of Ferric Citrate versus Ferrous Sulfate on Iron and Phosphate Parameters in Patients with Iron Deficiency and CKD

2020 ◽  
Vol 15 (9) ◽  
pp. 1251-1258 ◽  
Author(s):  
Rebecca Womack ◽  
Fabian Berru ◽  
Bhupesh Panwar ◽  
Orlando M. Gutiérrez
Keyword(s):  
Iron Deficiency ◽  
Ferrous Sulfate ◽  
Fibroblast Growth Factor 23 ◽  
Transferrin Saturation ◽  
Ferric Citrate ◽  
Deficiency Anemia ◽  
Clinical Trial Registry ◽  
Severe Chronic Kidney Disease ◽  
Registration Number ◽  
Iron Parameters

Background and objectivesFerric citrate is an oral medication approved for treatment of iron deficiency anemia in patients with CKD not requiring dialysis. The relative efficacy of ferric citrate versus ferrous sulfate in treating iron deficiency in patients with CKD is unclear.Design, setting, participants, & measurementsWe randomized 60 adults with moderate to severe CKD (eGFR 15–45 ml/min per 1.73 m2) and iron deficiency (transferrin saturation [TSAT] ≤30% and ferritin ≤300 ng/ml) to ferric citrate (2 g three times a day with meals, n=30) or ferrous sulfate (325 mg three times a day, n=30) for 12 weeks. Primary outcomes were change in TSAT and ferritin from baseline to 12 weeks. Secondary outcomes were change in hemoglobin, fibroblast growth factor 23 (FGF23), and hepcidin.ResultsBaseline characteristics were well balanced between study arms. There was a greater increase in TSAT (between-group difference in mean change, 8%; 95% confidence interval [95% CI], 1 to 15; P=0.02) and ferritin (between-group difference in mean change, 37 ng/ml; 95% CI, 10 to 64; P=0.009) from baseline to 12 weeks in participants randomized to ferric citrate as compared with ferrous sulfate. Similarly, as compared with ferrous sulfate, treatment with ferric citrate resulted in a greater increase in hepcidin from baseline to 12 weeks (between-group difference, 69 pg/ml; 95% CI, 8 to 130). There were no between-group differences in mean change for hemoglobin (0.3 g/dl; 95% CI, −0.2 to 0.8), intact FGF23 (−29 pg/ml; 95% CI, −59 to 0.1), or C-terminal FGF23 (61 RU/ml; 95% CI, −181 to 58). The incidence of adverse events did not differ between treatment arms.ConclusionsAs compared with ferrous sulfate, treatment with ferric citrate for 12 weeks resulted in a greater mean increase in TSAT and ferritin concentrations in individuals with moderate to severe CKD and iron deficiency.Clinical Trial registry name and registration numberImpact of Ferric Citrate vs Ferrous Sulfate on Iron Parameters and Hemoglobin in Individuals With Moderate to Severe Chronic Kidney Disease (CKD) With Iron Deficiency, NCT02888171.

scholarly journals Iron parameters in patients with end-stage renal disease receiving lanthanum carbonate or other non-iron-based phosphate binders: Results from a phase 3, randomized open-label study

2018 ◽  
Vol 6 ◽  
pp. 205031211878616
Author(s):  
Rosamund J Wilson ◽  
Beverly Jones ◽  
Claudio Marelli
Keyword(s):  
Renal Disease ◽  
End Stage Renal Disease ◽  
Standard Therapy ◽  
Transferrin Saturation ◽  
Lanthanum Carbonate ◽  
Phosphate Binders ◽  
Iron Parameters ◽  
Iron Based ◽  
Stage Renal Disease ◽  
End Stage

Objectives: The recent availability of iron-based phosphate binders has raised some concerns about iron overload in patients with end-stage renal disease. This study evaluated iron parameters in patients with end-stage renal disease receiving lanthanum carbonate or other non-iron-based phosphate binders. Methods: This analysis used 2-year follow-up data from an open-label, multicentre, randomized, active-controlled, parallel-group, phase 3 trial of lanthanum carbonate (SPD405-307). After a washout period, if patients’ serum phosphate levels exceeded 5.9 mg/dL, they were randomized 1:1 to receive lanthanum carbonate (375–3000 mg/day) or non-iron-based standard therapy during a 6-week dose titration period. Patients achieving control of serum phosphate levels (⩽5.9 mg/dL) received maintenance therapy with lanthanum carbonate or standard therapy for up to 24 months. Results: No clinically relevant changes in mean (standard deviation) iron parameters between the treatment groups (lanthanum carbonate, n = 682; standard therapy, n = 677) from baseline to month 24/final visit were observed: iron (µg/dL), −1.1 (41.8) versus 1.0 (38.7); ferritin (ng/mL), 208.4 (445.1) versus 262.4 (505.5); transferrin saturation (%), 2.8 (18.0) versus 2.8 (17.3); and haemoglobin (g/dL), 0.4 (1.9) versus 0.3 (1.7), respectively (all, p > 0.1). There were no clinically relevant changes in the percentage of patients receiving any anti-anaemic preparation in either treatment group (pre- vs post-randomization: lanthanum carbonate, 94.9% vs 97.8%; standard therapy, 95.1% vs 98.8%, respectively). This is in contrast to the study by Lewis and colleagues, which found significant increases in ferritin and transferrin saturation levels in patients receiving ferric citrate versus active control (calcium acetate and/or sevelamer carbonate) after 52 weeks of therapy. Although serum ferritin and transferrin saturation are the recommended iron indices by the Kidney Disease Outcome Quality Initiative, they are indirect indicators of iron status. Longer-term studies are required to understand fully the potential risks associated with iron overload. Conclusion: No evidence of iron accumulation was found in patients with end-stage renal disease receiving lanthanum carbonate or other non-iron-based binders.

scholarly journals Iron Deficiency and Erythropoiesis: New Diagnostic Approaches

2003 ◽  
Vol 49 (10) ◽  
pp. 1573-1578 ◽  
Author(s):  
Carlo Brugnara
Keyword(s):  
Chronic Disease ◽  
Iron Deficiency ◽  
Transferrin Saturation ◽  
Microcytic Anemia ◽  
Deficiency Anemia ◽  
Anemia Of Chronic Disease ◽  
Body Iron ◽  
Iron Stores ◽  
Human Erythropoietin ◽  
Iron Deficient

Abstract Iron deficiency anemia is one of the most common diseases worldwide. In the majority of cases, the presence of hypochromic microcytic anemia and biochemical evidence for depletion of body iron stores makes the diagnosis relatively straightforward. However, in several clinical conditions, classic biochemical indices such as serum iron, transferrin saturation, and ferritin may not be informative or may not change rapidly enough to reflect transient iron-deficient states (functional iron deficiency), such as the ones that develop during recombinant human erythropoietin (r-HuEPO) therapy. The identification and treatment of iron deficiency in settings such as r-HuEPO therapy, anemia of chronic disease, and iron deficiency of early childhood may be improved by the use of red cell and reticulocyte cellular indices, which reflect in almost real time the development of iron deficiency and the response to iron therapy. In the anemia of chronic disease, measurements of plasma cytokines and iron metabolism regulators such as hepcidin (when available) may be helpful in the characterization of the pathophysiologic basis of this condition. The ratio of serum transferrin receptor (sTfR) to serum ferritin (R/F ratio) has been shown to have excellent performance in estimating body iron stores, but it cannot be used widely because of the lack of standardization for sTfR assays. The combination of hematologic markers such as reticulocyte hemoglobin content, which decreases with iron deficiency, and R/F ratio may allow for a more precise classification of anemias.

The safety of achieved iron stores and their effect on IV iron and ESA use: post-hoc results from a randomized trial of ferric citrate as a phosphate binder in dialysis

2017 ◽  
Vol 87 (03) ◽  
pp. 124-133 ◽  
Author(s):  
Kausik Umanath ◽  
Barbara Greco ◽  
Diana Jalal ◽  
Molly McFadden ◽  
Mohammed Sika ◽  
...  
Keyword(s):  
Randomized Trial ◽  
Phosphate Binder ◽  
Ferric Citrate ◽  
Iron Stores ◽  
Iv Iron ◽  
Post Hoc

P0272COMPARATIVE GUT MICROBIOME DIFFERENCES BETWEEN FERRIC CITRATE AND CALCIUM CARBONATE PHOSPHATE BINDER TREATMENT IN HEMODIALYSIS PATIENTS

2020 ◽  
Vol 35 (Supplement_3) ◽  
Author(s):  
Ping-Hsun Wu ◽  
Yi-Ting Lin ◽  
Po-Yu Liu ◽  
Mei-Chuan Kuo ◽  
Yi wen Chiu
Keyword(s):  
Calcium Carbonate ◽  
Gut Microbiome ◽  
Phosphate Binder ◽  
Hemodialysis Patients ◽  
Ferric Citrate ◽  
Phosphate Binders ◽  
Uremic Toxin ◽  
Phosphate Binding ◽  
Microbial Composition ◽  
Linear Discriminant

Abstract Background and Aims Gut microbiome alteration increases uremic toxin levels inducing chronic inflammation and leading morbidity and mortality in patients with chronic kidney disease. Phosphate-binding agents may potentially change the composition of the gut microbiota. However, the limited clinical study investigates the microbiome difference between iron-containing and calcium-containing phosphate binders. The aim of this study was to compare the microbiota composition in hemodialysis patients treated with ferric citrate or calcium carbonate. Method The stool microbiota was investigated in hemodialysis patients with ferric citrate used (n=8) and calcium carbonate used (n=46) by 16S rRNA next-generation gene sequencing profiling. The altered microbiota between two different phosphate binders was analyzed. Differences in the microbial composition of the two patient groups were assessed using linear discriminant analysis effect size. Results Hemodialysis patients with calcium carbonate used revealed significantly reduced microbial species diversity (Shannon index and Simpson index) and increased microbial dysbiosis index compared with ferric citrate users. Compared to patients taking calcium carbonate, a distinct microbial community structure in patients taking ferric citrate, with an increased abundance of Bacteroidetes phylum and decreased abundance of phylum Firmicutes. In comparison between two phosphate binder users, members of the order Lactobacillales were prominent in calcium carbonate therapy, including family Streptococcaceae and genus Streptococcus. In contrast, taxa of the genus Ruminococcaceae, Flavonifractor, and Cronobacter were enriched in ferric citrate phosphate binder users. Conclusion The fecal microbiota was richer and more diverse in the ferric citrate group than in the calcium carbonate group. Hemodialysis patients with ferric citrate used were associated with differences in the gut microbiome composition compared to calcium carbonate users.

scholarly journals Comparative Gut Microbiome Differences between Ferric Citrate and Calcium Carbonate Phosphate Binders in Patients with End-Stage Kidney Disease

2020 ◽  
Vol 8 (12) ◽  
pp. 2040
Author(s):  
Ping-Hsun Wu ◽  
Po-Yu Liu ◽  
Yi-Wen Chiu ◽  
Wei-Chun Hung ◽  
Yi-Ting Lin ◽  
...  
Keyword(s):  
Calcium Carbonate ◽  
Kidney Disease ◽  
Gut Microbiome ◽  
Phosphate Binder ◽  
Hemodialysis Patients ◽  
Ferric Citrate ◽  
Phosphate Binders ◽  
Rrna Gene ◽  
Phosphate Binding ◽  
Linear Discriminant

Gut dysbiosis in patients with chronic kidney disease (CKD) may induce chronic inflammation and increase morbidity. Phosphate-binding agents, generally used in patients with CKD, may potentially change the composition of the gut microbiota. This study aimed to compare the microbiota composition in hemodialysis patients treated with ferric citrate or calcium carbonate. The stool microbiota was investigated in hemodialysis patients treated with ferric citrate (n = 8) and calcium carbonate (n = 46) using 16S rRNA gene amplicon sequencing profiling using linear discriminant analysis of effect size. Further predictive functional profiling of microbial communities was obtained with Tax4Fun in R. Hemodialysis patients treated with calcium carbonate had a significantly reduced microbial species diversity (Shannon index and Simpson index) and an increased microbial alteration ratio compared with patients treated with ferric citrate. A distinct microbial community structure was found in patients treated with ferric citrate, with an increased abundance of the Bacteroidetes phylum and a decreased abundance of the phylum Firmicutes. Members of the order Lactobacillales were enriched in patients treated with calcium carbonate, whereas taxa of the genera Ruminococcaceae UCG-004, Flavonifractor, and Cronobacter were enriched in patients treated with ferric citrate phosphate binder. In conclusion, Ferric citrate therapy results in a more diverse microbiome community compared to calcium carbonate therapy in hemodialysis patients with phosphate binder treatment. The gut microbiome reflects the phosphate binder choice in hemodialysis patients, further affecting the physiological environment in the gastrointestinal tract.

scholarly journals Myopia Control with Combination Low-Dose Atropine and Peripheral Defocus Soft Contact Lenses: A Case Series

2021 ◽  
pp. 548-554
Author(s):  
Nir Erdinest ◽  
Naomi London ◽  
Nadav Levinger ◽  
Yair Morad
Keyword(s):  
Low Dose ◽  
Contact Lenses ◽  
Case Series ◽  
Concentric Circle ◽  
Retrospective Case ◽  
Soft Contact ◽  
Myopia Progression ◽  
Soft Contact Lenses ◽  
Center Distance ◽  
Myopia Control

The goal of this retrospective case series is to demonstrate the effectivity of combination low-dose atropine therapy with peripheral defocus, double concentric circle design with a center distance soft contact lenses at controlling myopia progression over 1 year of treatment. Included in this series are 3 female children aged 8–10 years with progressing myopia averaging −4.37 ± 0.88 D at the beginning of treatment. Their average annual myopic progression during the 3 years prior to therapy was 1.12 ± 0.75 D. They had not attempted any myopia control treatments prior to this therapy. The children were treated with a combination of 0.01% atropine therapy with spherical peripheral defocus daily replacement soft lenses MiSight<sup>®</sup> 1 day (Cooper Vision, Phoenix, AZ, USA). They underwent cycloplegic refraction, and a slit-lamp evaluation every 6 months which confirmed no adverse reactions or staining was present. Each of the 3 children exhibited an average of 0.25 ± 0.25 D of myopia progression at the end of 1 year of treatment. To the best of the authors’ knowledge, this is the first published study exhibiting that combining low-dose atropine and peripheral defocus soft contact lenses is effective at controlling children’s moderate to severe myopia progression during 1 year of therapy.

scholarly journals Phosphate Control: The Next Frontier in Dialysis Cardiovascular Mortality

2021 ◽  
pp. 1-10
Author(s):  
Peter A. McCullough
Keyword(s):  
Calcium Acetate ◽  
Paracellular Pathway ◽  
Ferric Citrate ◽  
Morbidity And Mortality ◽  
Phosphate Binders ◽  
Phosphate Absorption ◽  
Phosphate Retention ◽  
Sevelamer Carbonate ◽  
Prescribing Information ◽  
Phosphate Control

<b><i>Background:</i></b> Cardiovascular disease (CVD) is a major cause of death in patients with chronic kidney disease (CKD) on dialysis. Mortality rates are still unacceptably high even though they have fallen in the past 2 decades. Hyperphosphatemia (elevated serum phosphate levels) is seen in almost all patients with advanced CKD and is by far the largest remaining modifiable contributor to CKD mortality. <b><i>Summary:</i></b> Phosphate retention drives multiple physiological mechanisms linked to increased risk of CVD. Fibroblast growth factor 23 and parathyroid hormone (PTH) levels, both of which have been suggested to have direct pathogenic CV effects, increase in response to phosphate retention. Phosphate, calcium, and PTH levels are linked in a progressively worsening cycle. Maladaptive upregulation of phosphate absorption is also likely to occur further exacerbating hyperphosphatemia. Even higher phosphate levels within the normal range may be a risk factor for vascular calcification and, thus, CV morbidity and mortality. A greater degree of phosphate control is important to reduce the risk of CV morbidity and mortality. Improved phosphate control and regular monitoring of phosphate levels are guideline-recommended, established clinical practices. There are several challenges with the current phosphate management approaches in patients with CKD on dialysis. Dietary restriction of phosphate and thrice-weekly dialysis alone are insufficient/unreliable to reduce phosphate to &#x3c;5.5 mg/dL. Even with the addition of phosphate binders, the only pharmacological treatment currently indicated for hyperphosphatemia, the majority of patients are unable to achieve and maintain phosphate levels &#x3c;5.5 mg/dL (or more normal levels) [PhosLo® gelcaps (calcium acetate): 667 mg (prescribing information), 2011, VELPHORO®: (Sucroferric oxyhydroxide) (prescribing information), 2013, FOSRENAL®: (Lanthanum carbonate) (prescribing information), 2016, AURYXIA®: (Ferric citrate) tablets (prescribing information), 2017, RENVELA®: (Sevelamer carbonate) (prescribing information), 2020, RealWorld dynamix. Dialysis US: Spherix Global Insights, 2019]. Phosphate binders do not target the primary pathway of phosphate absorption (paracellular), have limited binding capacity, and bind nonspecifically [PhosLo® gelcaps (calcium acetate): 667 mg (prescribing information). 2013, VELPHORO®: (Sucroferric oxyhydroxide) (prescribing information), 2013, FOSRENAL®: (Lanthanum carbonate) (prescribing information), 2016, AURYXIA®: (Ferric citrate) tablets (prescribing information), 2017, RENVELA®: (Sevelamer carbonate) (prescribing information) 2020]. <b><i>Key Messages:</i></b> Despite current phosphate management strategies, most patients on dialysis are unable to consistently achieve target phosphate levels, indicating a need for therapeutic innovations [RealWorld dynamix. Dialysis US: Spherix Global Insights, 2019]. Given a growing evidence base that the dominant mechanism of phosphate absorption is the intestinal paracellular pathway, new therapies are investigating ways to reduce phosphate levels by blocking absorption through the paracellular pathway.

Sign in / Sign up

Export Citation Format

Share Document