Determinants of progressive vascular calcification in haemodialysis patients

被引:234
作者
Chertow, GM
Raggi, P
Chasan-Taber, S
Bommer, J
Holzer, H
Burke, SK
机构
[1] Univ Calif San Francisco, Dept Med, Mt Zion Med Ctr, San Francisco, CA USA
[2] Moffitt Long Hosp, Div Nephrol, San Francisco, CA USA
[3] Tulane Univ, Dept Med, Div Cardiol, New Orleans, LA 70118 USA
[4] Pioneer BioDiligence, Amherst, MA USA
[5] Univ Klinikum Heidelberg, Heidelberg, Germany
[6] Univ Klinikum Graz, Graz, Austria
[7] Genzyme Drug Discovery & Dev, Waltham, MA USA
关键词
calcium; ESRD; haemodialysis; PTH; sevelamer;
D O I
10.1093/ndt/gfh125
中图分类号
R3 [基础医学]; R4 [临床医学];
学科分类号
1001 ; 1002 ; 100602 ;
摘要
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.
引用
收藏
页码:1489 / 1496
页数:8
相关论文
共 30 条
[1]   Variability of repeated coronary artery calcium measurements by electron beam tomography [J].
Achenbach, S ;
Ropers, D ;
Möhlenkamp, S ;
Schmermund, A ;
Muschiol, G ;
Groth, J ;
Kusus, M ;
Regenfus, M ;
Daniel, WG ;
Erbel, R ;
Moshage, W .
AMERICAN JOURNAL OF CARDIOLOGY, 2001, 87 (02) :210-+
[2]   QUANTIFICATION OF CORONARY-ARTERY CALCIUM USING ULTRAFAST COMPUTED-TOMOGRAPHY [J].
AGATSTON, AS ;
JANOWITZ, WR ;
HILDNER, FJ ;
ZUSMER, NR ;
VIAMONTE, M ;
DETRANO, R .
JOURNAL OF THE AMERICAN COLLEGE OF CARDIOLOGY, 1990, 15 (04) :827-832
[3]   Arterial calcifications, arterial stiffness, and cardiovascular risk in end-stage renal disease [J].
Blacher, J ;
Guerin, AP ;
Pannier, B ;
Marchais, SJ ;
London, GM .
HYPERTENSION, 2001, 38 (04) :938-942
[4]   Association of serum phosphorus and calcium x phosphate product with mortality risk in chronic hemodialysis patients: A national study [J].
Block, GA ;
Hulbert-Shearon, TE ;
Levin, NW ;
Port, FK .
AMERICAN JOURNAL OF KIDNEY DISEASES, 1998, 31 (04) :607-617
[5]   Electron beam computed tomography in the evaluation of cardiac calcifications in chronic dialysis patients [J].
Braun, J ;
Oldendorf, M ;
Moshage, W ;
Heidler, R ;
Zeitler, E ;
Luft, FC .
AMERICAN JOURNAL OF KIDNEY DISEASES, 1996, 27 (03) :394-401
[6]   Effect of HMG-Coa reductase inhibitors on coronary artery disease as assessed by electron-beam computed tomography [J].
Callister, TQ ;
Raggi, P ;
Cooil, B ;
Lippolis, NJ ;
Russo, DJ .
NEW ENGLAND JOURNAL OF MEDICINE, 1998, 339 (27) :1972-1978
[7]   Sevelamer attenuates the progression of coronary and aortic calcification in hemodialysis patients [J].
Chertow, GM ;
Burke, SK ;
Raggi, P .
KIDNEY INTERNATIONAL, 2002, 62 (01) :245-252
[8]   Pathophysiological mechanisms of vascular calcification in end-stage renal disease [J].
Davies, MR ;
Hruska, KA .
KIDNEY INTERNATIONAL, 2001, 60 (02) :472-479
[9]   On the evolving nature of understanding dialysis-related disorders [J].
Eknoyan, G ;
Lindberg, JS .
AMERICAN JOURNAL OF KIDNEY DISEASES, 2003, 41 (04) :S1-S3
[10]  
FRIEDEWALD WT, 1972, CLIN CHEM, V18, P499