NDT Advance Access originally published online on November 1, 2005
Nephrology Dialysis Transplantation 2006 21(3):707-714; doi:10.1093/ndt/gfi236
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© The Author [2005]. Published by Oxford University Press on behalf of ERA-EDTA. All rights reserved. For Permissions, please email: journals.permissions@oxfordjournals.org
Original Articles: Clinical Nephrology
Vascular calcification and cardiovascular function in chronic kidney disease
1 Department of Renal Medicine and 2 Department of Imaging, Derby City General Hospital, Derby, DE22 3NE, UK and 3 Centre for Integrated Systems Biology and Medicine, The University of Nottingham, UK
Correspondence and offprint requests to: Dr C. W. McIntyre, Department of Renal Medicine, Derby City General Hospital, Derby, DE22 3NE, UK. Email: Chris.McIntyre{at}derbyhospitals.nhs.uk
Background. Vascular calcification and arterial stiffening are independent predictors of all causes and cardiovascular mortality in chronic kidney disease (CKD). Few data are currently available comparing vascular calcification and its attendant functional cardiovascular consequences between CKD stage 4 patients and both peritoneal dialysis (PD) and haemodialysis (HD) (CKD stage 5) patients.
Method. We studied 134 subjects (60 HD, 28 PD and 46 CKD 4). Vascular calcification was quantified using multi-slice spiral CT scanning of a 5 cm standardized segment of superficial femoral artery. Pulse wave analysis and pulse wave velocity were assessed using applanation tonometry, to determine arterial compliance. Further digital arterial pulse wave analysis was used to measure systemic haemodynamic variables. All medications were recorded and biochemical variables were time averaged for the 6 months prior to entering the study.
Results. Forty-seven percent of CKD 4 patients demonstrated vascular calcification as compared with CKD 5 (71% PD and 73% HD, P = 0.02). HD patients had higher calcification scores (median 121) than either PD (median 21) or CKD 4 (median 0) (P = 0.008). There were no significant differences in baseline characteristics between the groups. Comparing tertiles of patients (based on calcification score), increased calcification score was associated with a reduction in arterial compliance (mean PWV 8.9±1.1, 11±3.6, 11.3±3.7 m/s, P = 0.005). The degree of calcification did not influence systolic blood pressure (BP), diastolic BP or heart rate. However, more heavily calcified patients demonstrated significantly higher mean pulse pressures (58±19, 74±22 and 72±25 mmHg, P = 0.001), lower total peripheral resistance (1.5±1, 1.3±0.8, 0.9±0.4, P = 0.01) and higher stroke volume (84±25, 95±29, 106±39 ml, P = 0.01). More heavily calcified patients were significantly older and predominantly male.
Conclusion. This study has successfully utilized a novel technique for the quantification of calcification. We have demonstrated vascular calcification and associated cardiovascular dysfunction in CKD 4, PD and HD with significant differences between the groups. Thirty percent of individuals show no calcification, even those established on renal replacement therapy for a prolonged period of time. Further work is required to identify factors which promote progression of arterial calcification in those who are susceptible.
Keywords: arterial stiffness; calcification; cardiovascular mortality; chronic kidney failure; haemodialysis; haemodynamics; peritoneal dialysis; phosphate binder
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