Vascular calcification and cardiovascular function in chronic kidney disease

• Published in: Nephrology, dialysis, transplantation Vol. 21; no. 3; pp. 707 - 714
• Main Authors: Sigrist, Mhairi, Bungay, Peter, Taal, Maarter W., McIntyre, Christopher W.
• Format: Journal Article
• Language: English
• Published: Oxford Oxford University Press 01.03.2006; Oxford Publishing Limited (England)
• Subjects: Anesthesia. Intensive care medicine. Transfusions. Cell therapy and gene therapy; arterial stiffness; Biological and medical sciences; calcification; Calcinosis - etiology; Calcinosis - mortality; Calcinosis - physiopathology; cardiovascular mortality; chronic kidney failure; Cross-Sectional Studies; Emergency and intensive care: renal failure. Dialysis management; Female; Femoral Artery - diagnostic imaging; Femoral Artery - physiopathology; haemodialysis; haemodynamics; Humans; Intensive care medicine; Kidney Failure, Chronic - complications; Kidney Failure, Chronic - therapy; Kidneys; Male; Medical sciences; Middle Aged; Nephrology. Urinary tract diseases; Nephropathies. Renovascular diseases. Renal failure; peritoneal dialysis; phosphate binder; Renal Dialysis; Renal failure; Retrospective Studies; Risk Factors; Survival Rate; Tomography, X-Ray Computed; Tumors of the urinary system; Vascular Diseases - diagnostic imaging; Vascular Diseases - etiology; Vascular Diseases - physiopathology; Vascular Resistance - physiology; Kidney disease; Phosphates; arterial stiffness; Urinary system disease; Hemodialysis; Mortality; cardiovascular mortality; haemodialysis; Cardiovascular disease; phosphate binder; Binders; chronic kidney failure; Peritoneal dialysis; Extrarenal dialysis; Renal failure; Calcification; Stiffness; Hemodynamics; haemodynamics
• ISSN: 0931-0509; 1460-2385
• DOI: 10.1093/ndt/gfi236

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.