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NDT Advance Access published online on July 2, 2009

Nephrology Dialysis Transplantation, doi:10.1093/ndt/gfp325
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© The Author [2009]. Published by Oxford University Press on behalf of ERA-EDTA. All rights reserved. For Permissions, please e-mail: journals.permissions@oxfordjournals.org



Long-term mortality and cardiovascular risk stratification of peritoneal dialysis patients using a combination of inflammation and calcification markers

Angela Yee-Moon Wang1,3, Christopher Wai-Kei Lam2, Iris Hiu-Shuen Chan2, Mei Wang1,3, Siu-Fai Lui1 and John E. Sanderson1,4

1 Department of Medicine and Therapeutics 2 Department of Chemical Pathology, The Chinese University of Hong Kong, Prince of Wales Hospital, Shatin, New Territories, Hong Kong; Macau Institute for Applied Research in Medicine and Health, Macau University of Science and Technology Foundation, Taipa, Macau 3 Department of Medicine, Queen Mary Hospital, University of Hong Kong, Hong Kong 4 Department of Cardiovascular Medicine, The Medical School, University of Birmingham, Birmingham, UK

Correspondence and offprint requests to: Angela Yee-Moon Wang; E-mail: aymwang{at}hku.hk



  Abstract

Background. It remains unknown whether a composite of inflammation and calcification markers provides better mortality and cardiovascular risk stratification in chronic peritoneal dialysis (PD) patients.

Methods. We performed a 4-year prospective follow-up study in 231 chronic PD patients from a single regional dialysis centre in Hong Kong. Valvular calcification was detected using echocardiography, and fasting venous blood was collected to measure a panel of inflammation markers. The patients were stratified into five groups on the basis of 0, 1, 2, 3 and all 4 inflammation and calcification risk markers, namely high C-reactive protein (CRP) (CRP in upper tertile), high interleukin-6 (IL-6) (IL-6 in upper tertile), low fetuin-A (fetuin-A in lower tertile) and valvular calcification. Study outcomes included all-cause and cardiovascular mortality and fatal or non-fatal cardiovascular events (CVEs).

Results. The patients with 4, 3, 2 and 1 markers had an adjusted hazard ratio (HR) of 5.17 (95% CI, 1.81–14.77, P = 0.002), 3.38 (95% CI, 1.50–7.60; P = 0.003), 2.17 (95% CI, 0.98–4.77; P = 0.056) and 2.42 (95% CI, 1.18–4.96; P = 0.016), respectively, for mortality at 4 years than those with 0 risk marker. The adjusted HRs for fatal or non-fatal CVEs were 4.33 (95% CI, 1.70–11.03; P = 0.002), 1.60 (95% CI, 0.73–3.52; P = 0.24), 1.92 (95% CI, 0.95–3.90; P = 0.07) and 1.33 (95% CI, 0.67–2.62; P = 0.42), respectively, for patients with 4, 3, 2 and 1 markers than those with 0 risk markers.

Conclusions. A composite of inflammation and calcification markers provides long-term prognostication and identifies the sickest PD patients with the worst clinical outcomes. Since these parameters can all be obtained quite readily, our data support the adoption of a multiinflammation and calcification risk marker approach for mortality and cardiovascular risk stratification in PD patients.

Keywords: calcification; cardiovascular events; inflammation; mortality; peritoneal dialysis

Received for publication: 25. 4.09
Accepted in revised form: 11. 6.09


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