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Updated: Jun 9, 2026

Calcification of Vascular Smooth Muscle Cells and Imaging of Aortic Calcification and Inflammation
Published on: May 31, 2016
Determinants of progressive vascular calcification in haemodialysis patients
Glenn M Chertow1, Paolo Raggi, Scott Chasan-Taber
1Division of Nephrology, Moffitt-Long Hospitals and UCSF-Mt. Zion Medical Center, Department of Medicine, University of California San Francisco, 94118-1211, USA. chertowg@medicine.ucsf.edu
Insights
Calcium-based phosphate binders worsen vascular calcification, especially with uncontrolled mineral metabolism. Sevelamer offers a safer alternative, potentially impacting lipids and calcification differently.
Area of Science:
- Nephrology
- Cardiovascular Medicine
- Mineral Metabolism
Background:
- Calcium-based phosphate binders (calcium acetate, carbonate) linked to progressive coronary artery and aortic calcification.
- Non-calcium binder, sevelamer, did not show this association.
- Hypothesized other factors beyond calcium influence calcification progression.
Purpose of the Study:
- Investigate determinants of progressive vascular calcification.
- Compare factors influencing calcification in calcium-binder vs. sevelamer groups.
Main Methods:
- 150 randomized subjects underwent electron beam tomography (EBT) at baseline and follow-up.
- Explored associations between mineral levels, parathyroid hormone (PTH), albumin, and calcification progression.
- Analyzed data separately for calcium-binder and sevelamer treatment groups.
Main Results:
- Higher calcium, phosphorus, and calcium-phosphorus product correlated with increased EBT scores in calcium-treated subjects.
- No such association found in sevelamer-treated subjects.
- PTH showed complex associations; albumin inversely correlated with aortic calcification progression. Sevelamer improved lipids.
Conclusions:
- Calcium-based binders promote vascular calcification, particularly with poor mineral control.
- Calcium may negatively impact skeletal and extraskeletal calcification, potentially via PTH.
- Sevelamer demonstrates a potentially favorable profile regarding vascular calcification and lipids.
Background:
We determined recently that targeted treatment with calcium-based phosphate binders (calcium acetate and carbonate) led to progressive coronary artery and aortic calcification by electron beam tomography (EBT), while treatment with the non-calcium-containing phosphate binder, sevelamer, did not. Aside from the provision of calcium, we hypothesized that other factors might be related to the likelihood of progressive calcification in both or either treatment groups.
Methods:
We explored potential determinants of progressive vascular calcification in 150 randomized study subjects who underwent EBT at baseline and at least once during follow-up (week 26 or 52).
Results:
Among calcium-treated subjects, higher time-averaged concentrations of calcium, phosphorus and the calcium-phosphorus product were associated with more pronounced increases in EBT scores; no such associations were demonstrated in sevelamer-treated subjects. The relation between parathyroid hormone (PTH) and the progression of calcification was more complex. Lower PTH was associated with more extensive calcification in calcium-treated subjects, whereas higher PTH was associated with calcification in sevelamer-treated subjects. Serum albumin was inversely correlated with progression in aortic calcification. Sevelamer was associated with favourable effects on lipids, although the link between these effects and the observed attenuation in vascular calcification remains to be elucidated.
Conclusion:
Calcium-based phosphate binders are associated with progressive coronary artery and aortic calcification, especially when mineral metabolism is not well controlled. Calcium may directly or indirectly (via PTH) adversely influence the balance of skeletal and extraskeletal calcification in haemodialysis patients.
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Hemodialysis I: Introduction
Hemodialysis II: Procedure and Complications
Hemodialysis III: Nursing Management
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Chronic Kidney Disease II: Clinical Manifestations

