Determinants of progressive vascular calcification in haemodialysis patients.
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.


CONCLUSIONS
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.
Chertow
Glenn M
GM
Division 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
Raggi
Paolo
P
Chasan-Taber
Scott
S
Bommer
Juergen
J
Holzer
Herwig
H
Burke
Steven K
SK
D000368:Aged; D001161:Arteriosclerosis / Q000453:epidemiology* / Q000209:etiology*; D001808:Blood Vessels / Q000473:pathology*; D002114:Calcinosis / Q000453:epidemiology / Q000209:etiology*; D002118:Calcium / Q000097:blood*; D015897:Comorbidity; D018450:Disease Progression; D004852:Epoxy Compounds / Q000494:pharmacology*; D005260:Female; D006801:Humans; D007676:Kidney Failure, Chronic / Q000453:epidemiology / Q000628:therapy; D008297:Male; D010281:Parathyroid Hormone; D010710:Phosphates / Q000097:blood*; D011073:Polyamines; D011095:Polyethylenes / Q000494:pharmacology*; D006435:Renal Dialysis; D000069603:Sevelamer; D018709:Statistics, Nonparametric; D014057:Tomography, X-Ray Computed
D004852:Epoxy Compounds; D010281:Parathyroid Hormone; D010710:Phosphates; D011073:Polyamines; D011095:Polyethylenes; D000069603:Sevelamer; D002118:Calcium