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Pulse wave velocity and vascular calcification at different stages of chronic kidney disease

Temmar, Mohameda,b,*; Liabeuf, Sophiea,b,*; Renard, Cédricd; Czernichow, Sébastiene,f; Esper, Najeh Elc; Shahapuni, Irinac; Presne, Clairec; Makdassi, Raifahc; Andrejak, Michela,b; Tribouilloy, Christophea,g; Galan, Pilare,f; Safar, Michel Eh; Choukroun, Gabriela,c; Massy, Ziada,b,c

doi: 10.1097/HJH.0b013e328331b81e
Original papers: Kidney

Background Increased arterial stiffness and vascular calcification have been recognized as important predictors of cardiovascular mortality in patients with chronic kidney disease.

Method In order to examine the precise temporal link between aortic stiffness and cardiovascular risk at the earliest stages of chronic kidney disease, we studied a cohort of 150 patients with chronic kidney disease (52 stage 2/3 patients, 51 stage 4/5 patients and 47 stage 5D patients). Each patient underwent a plain, lateral lumbar radiograph and an abdominal and thoracic multislice spiral computer tomography scan in order to identify and quantify aortic and coronary calcifications. Pulse wave velocity was used as a measure of arterial stiffness.

Results Regardless of the disease stage, patients with chronic kidney disease had higher adjusted pulse wave velocity than controls with preserved renal function (14.6 ± 3.8 vs. 10.7 ± 1.7 m/s, respectively; P < 0.0001). Regarding aortic calcification, there was a gradual but significant rise in later chronic kidney disease stages. A similar trend was found for coronary calcification. In a multivariate analysis only age, mean arterial pressure, diabetes and the aortic calcification score were independent determinants of higher pulse wave velocity.

Conclusion We found that both vascular stiffness and vascular calcification appear early in patients with chronic kidney disease, but only vascular calcification worsens as the disease progresses. The increase of vascular stiffness in adult patients with chronic kidney disease seems to be more related to age, systolic blood pressure, diabetes and vascular calcification than to uremic toxicity.

aINSERM, ERI-12 (EA 4292), France

bClinical Research Centre - Division of Clinical Pharmacology, Amiens University Medical Center, and the Jules Verne University of Picardy, France

cDivision of Nephrology, France

dDivision of Radiology, Amiens University Medical Center, Amiens, France

eNutritional Epidemiology research Unit-UMR U557 INSERM, U1125 INRA, CNAM, Paris, CRNH-IdF, France

fPublic Health Department, Avicenne Hospital, Paris 13 University, Bobigny, France

gDivision of Cardiology, Amiens University Medical Center, Amiens, France

hParis-Descartes University, Faculty of Medicine, Hôtel-Dieu Hospital, AP-HP, Paris, France

* M.T. and S.L. contributed equally to the writing of the article.

Received 3 April, 2009

Revised 4 July, 2009

Accepted 10 August, 2009

Correspondence to Professor Ziad A. Massy, MD, PhD, INSERM ERI-12, University of Picardy and Amiens University Medical Center, Divisions of Clinical Pharmacology and Nephrology, Avenue René Laennec, F-80054 Amiens, France Tel: +33 322 455 788; fax: +33 322 455 660; e-mail:

© 2010 Lippincott Williams & Wilkins, Inc.