The effects of sevelamer and calcium acetate on proxies of atherosclerotic and arteriosclerotic vascular disease in hemodialysis patients.
BACKGROUND
We recently determined that in hemodialysis patients, the use of calcium salts to correct hyperphosphatemia led to progressive coronary artery and aortic calcification as determined by sequential electron beam tomography (EBT) while the use of the non-calcium-containing binder sevelamer did not. Whether the specific calcium preparation (acetate vs. carbonate) might influence the likelihood of progressive calcification was debated.


METHODS
To determine whether treatment with calcium acetate was specifically associated with hypercalcemia and progressive vascular calcification, we conducted an analysis restricted to 108 hemodialysis patients randomized to calcium acetate or sevelamer and followed for one year.


RESULTS
The reduction in serum phosphorus was roughly equivalent with both agents (calcium acetate -2.5 +/- 1.8 mg/dl vs. sevelamer -2.8 +/- 2.0 mg/dl, p = 0.53). Subjects given calcium acetate were more likely to develop hypercalcemia (defined as an albumin-corrected serum calcium > or =10.5 mg/dl) (36 vs. 13%, p = 0.015). Treatment with calcium acetate (mean 4.6 +/- 2.1 g/day - equivalent to 1.2 +/- 0.5 g of elemental calcium) led to a significant increase in EBT-determined calcification of the coronary arteries (mean change 182 +/- 350, median change +20, p = 0.002) and aorta (mean change 181 +/- 855, median change +73, p < 0.0001). These changes were similar in magnitude to those seen with calcium carbonate. There were no significant changes in calcification among sevelamer-treated subjects.


CONCLUSIONS
Despite purported differences in safety and efficacy relative to calcium carbonate, calcium acetate led to hypercalcemia and progressive vascular calcification in hemodialysis patients.
Chertow
Glenn M
GM
Division of Nephrology, Moffitt-Long Hospitals and UCSF-Mt. Zion Medical Center, Department of Medicine, University of California San Francisco, San Francisco, CA, USA. chertowg@medicine.ucsf.edu
Raggi
Paolo
P
McCarthy
James T
JT
Schulman
Gerald
G
Silberzweig
Jeffrey
J
Kuhlik
Amy
A
Goodman
William G
WG
Boulay
Amy
A
Burke
Steven K
SK
Toto
Robert D
RD
D000085:Acetates / Q000009:adverse effects / Q000494:pharmacology*; D000328:Adult; D001018:Aortic Diseases / Q000139:chemically induced*; D001161:Arteriosclerosis / Q000139:chemically induced*; D002114:Calcinosis / Q000517:prevention & control*; D002118:Calcium / Q000097:blood; D017610:Calcium Compounds; D004852:Epoxy Compounds / Q000009:adverse effects / Q000494:pharmacology*; D005260:Female; D006801:Humans; D006934:Hypercalcemia / Q000139:chemically induced*; D008297:Male; D008875:Middle Aged; D010710:Phosphates / Q000097:blood*; D011073:Polyamines; D011095:Polyethylenes / Q000009:adverse effects / Q000494:pharmacology*; D006435:Renal Dialysis / Q000009:adverse effects*; D000069603:Sevelamer; D018709:Statistics, Nonparametric
D000085:Acetates; D017610:Calcium Compounds; D004852:Epoxy Compounds; D010710:Phosphates; D011073:Polyamines; D011095:Polyethylenes; D000069603:Sevelamer; D002118:Calcium; C120662:calcium acetate