Effect of Phosphate Binders on Markers of Vascular Health in Chronic Kidney Disease Stages 3 and 4

A Randomized Study on the Effects of Sevelamer Carbonate Versus Calcium Acetate on Biomarkers of Vascular Calcification, Inflammation, and Endothelial Dysfunction in Chronic Kidney Disease Stages 3 and 4

Status

Terminated

Phases

Phase 4

Study type

Interventional

Source

ClinicalTrials.gov

Registry ID

NCT01277497

Enrollment

Registered

2011-01-17

Start date

2011-01-31

Completion date

2016-03-31

Last updated

2016-01-14

For informational purposes only — not medical advice. Sourced from public registries and may not reflect the latest updates. Terms

Conditions

Chronic Kidney Disease

Keywords

Chronic kidney disease, Phosphate binder, Sevelamer carbonate, Calcium acetate, Vascular calcification, Endothelial Dysfunction

Brief summary

Chronic kidney disease (CKD) patients often have high levels of a substance called fibroblast growth factor-23 (FGF-23), a phosphorus excreting hormone, which has been related to heart disease. As kidney function declines, less phosphorus is removed by the kidneys and as a result phosphorus accumulates in the blood. In response to elevated phosphorus levels, more FGF-23 is released to help facilitate the excretion of extra phosphorus into the urine. In addition to effects on FGF-23, increased phosphorus levels can lead to calcification (hardening) of the blood vessels in the CKD population. Phosphate binding medicines are used in CKD patients to lower the amount of phosphorus absorbed by the stomach and intestines after eating meals and snacks. In patients with CKD, studies have shown that phosphate binders can lower FGF-23 levels in the blood. Lowering FGF-23 levels in CKD patients may also lower substances in the blood that cause calcification of blood vessels in the CKD population. This study is being done to determine if using phosphate binders, either sevelamer carbonate or calcium acetate, in the earlier stages kidney disease (before dialysis) can decrease FGF-23 and biomarkers (substances in the blood) associated with hardening of the blood vessels and heart disease.

Interventions

DRUGSevelamer carbonate

Sevelamer carbonate 1,600 mg three times daily with meals

DRUGCalcium acetate

Calcium acetate 1,334 mg three times daily with meals for 12 weeks

Study design

Allocation

RANDOMIZED

Intervention model

PARALLEL

Primary purpose

PREVENTION

Masking

NONE

Eligibility

Sex/Gender

ALL

Age

18 Years to No maximum

Healthy volunteers

Inclusion criteria

* Males or females ≥ 18 years of age at start of screening * CKD stage 3 or 4 defined by an eGFR 15 - 60 mL/min/1.73m2 * Not expected to start dialysis for 8 months * Serum intact PTH \< 500 pg/mL during screening period * On a stable ACE inhibitor/ARB regimen for 30 days prior to screening

Exclusion criteria

* History of any of the following diseases: congestive heart failure, MI within the last 6 months, cerebrovascular accident, significant valvular disease, malignancy * Currently receiving erythropoiesis stimulating agent or IV iron therapy * History of inflammatory/autoimmune disease * History of polycystic kidney disease * HIV positive or AIDS * Pregnant or breastfeeding * Receiving activated Vitamin D analogs, nutritional vitamin D agents \> 2,000 IU/day, or calcimimetics with in the last 3 months * Significant GI disorder * Proteinuria \>3.5 g/24 hours

Design outcomes

Primary

Measure	Time frame
The primary outcome measure will be the change in FGF-23 concentrations	12 weeks

Secondary

Measure	Time frame
Change in vascular calcification biomarker levels	12 weeks
Change in endothelial dysfunction biomarker levels.	12 Weeks
Change in inflammatory biomarker levels	12 Weeks

Countries

United States

Outcome results

None listed

Source: ClinicalTrials.gov · Data processed: Feb 4, 2026