NDT Advance Access originally published online on February 27, 2006
Nephrology Dialysis Transplantation 2006 21(5):1407-1412; doi:10.1093/ndt/gfl021
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The natural history of coronary calcification progression in a cohort of nocturnal haemodialysis patients
1 Department of Medicine, Division of Nephrology, Toronto General Hospital – University Health Network, University of Toronto and 2 Division of Nephrology, Humber River Regional Hospital, University of Toronto, Canada
Correspondence and offprint requests to: Dr Christopher T. Chan, North Wing 8 – 842, Toronto General Hospital, University Health Network, 200 Elizabeth Street, Toronto, ON, Canada M5G 2C4. Email: christopher.chan{at}uhn.on.ca
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.
Keywords: calcium; coronary calcification; nocturnal haemodialysis; phosphate; parathyroid hormone
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