The natural history of coronary calcification progression in a cohort of nocturnal haemodialysis patients

被引:59
作者
Yuen, D
Pierratos, A
Richardson, RMA
Chan, CT
机构
[1] Univ Toronto, Toronto Gen Hosp, Hlth Network, Dept Med,Div Nephrol, Toronto, ON M5G 2C4, Canada
[2] Univ Toronto, Humber River Reg Hosp, Div Nephrol, Toronto, ON M5G 2C4, Canada
关键词
calcium; coronary calcification; nocturnal haemodialysis; phosphate; parathyroid hormone;
D O I
10.1093/ndt/gfl021
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. End-stage renal disease (ESRD) is associated with a markedly increased cardiac calcification burden, as reflected by computed tomography scans of the heart. Nocturnal haemodialysis (NHD) is a novel form of renal replacement therapy which has multiple physiologic effects that may affect vascular calcification, including improvements in phosphate and uraemia control. The objective of the present study is the determination of the natural history of coronary calcification progression in patients converted to NHD, and the examination of the relationships between calcification risk factors and calcification progression in these patients. Methods. Thirty-eight ESRD patients were converted to NHD, and included in our observational cohort study. Coronary artery calcification scores (CACS) were documented at baseline and post-conversion (mean interscan duration 16 +/- 1 months). Other variables of interest included age, dialysis vintage, Framingham risk profile, phosphate binder and vitamin D usage, and plasma levels of calcium, phosphate and parathyroid hormone. Results. Our cohort was stratified according to baseline calcification burden (minimal calcification: CACS <= 10 vs significant calcification: CACS > 10). Twenty-four patients had baseline CACS <= 10. These patients demonstrated no change in coronary calcification after 1 year of NHD (from 0.7 +/- 0.5 to 6 +/- 3, P = 0.1). Fourteen patients had higher initial CACS at baseline (1874 +/- 696), and demonstrated a non-significant 9% increase over 1 year to 2038 +/- 740 (P = 0.1). Plasma phosphate and calcium x phosphate product were significantly reduced, as were calcium-based phosphate binder and antihypertensive usage. Conclusions. Our study is the first to document CACS progression in a cohort of NHD patients. Further analysis of the effect of NHD on the physiology of cardiovascular calcification is required.
引用
收藏
页码:1407 / 1412
页数:6
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