title: Large artery stiffening and remodeling are independently associated with all-cause mortality and cardiovascular events in chronic kidney disease.
abstract: Chronic kidney disease, even at moderate stages, is characterized by a high incidence of cardiovascular events. Subclinical damage to large arteries, such as increased arterial stiffness and outward remodeling, is a classical hallmark of patients with chronic kidney disease. Whether large artery stiffness and remodeling influence the occurrence of cardiovascular events and the mortality of patients with chronic kidney disease (stages 2-5) is still debated. This prospective study included 439 patients with chronic kidney disease (mean age, 59.8 ± 14.5 years) with a mean measured glomerular filtration rate of 37 mL/min per 1.73 m(2). Baseline aortic stiffness was estimated through carotid-femoral pulse wave velocity measurements; carotid stiffness, diameter, and intima-media thickness were measured with a high-resolution echotracking system. For the overall group of patients, the 5-year estimated survival and cumulative incidence of cardiovascular events were 87% and 16%, respectively. In regression analyses adjusted on classical cardiovascular and renal risk factors, aortic stiffness remained significantly associated with all-cause mortality (for 1 SD, Cox model-derived relative risk [95% CI], 1.48 [1.09-2.02]) and with fatal and nonfatal cardiovascular events (for 1 SD, Fine and Gray competing risks model-derived relative risk [95% CI], 1.35 [1.05-1.75]). Net reclassification improvement index was significant (29.0% [2.3-42.0%]). Carotid internal diameter was also independently associated with all-cause mortality. This study shows that increased aortic stiffness and carotid internal diameter are independent predictors of mortality in patients with stages 2 to 5 chronic kidney disease and that aortic stiffness improves the prediction of the risk.
authors.affiliation: Departments of Nephrology, Hôpital Européen Georges Pompidou, Assistance Publique-Hôpitaux de Paris, Paris, France.
authors.forename: Alexandre
authors.initials: A
authors.lastname: Karras
authors.forename: Jean-Philippe
authors.initials: JP
authors.lastname: Haymann
authors.forename: Erwan
authors.initials: E
authors.lastname: Bozec
authors.forename: Marie
authors.initials: M
authors.lastname: Metzger
authors.forename: Christian
authors.initials: C
authors.lastname: Jacquot
authors.forename: Gerard
authors.initials: G
authors.lastname: Maruani
authors.forename: Pascal
authors.initials: P
authors.lastname: Houillier
authors.forename: Marc
authors.initials: M
authors.lastname: Froissart
authors.forename: Bénédicte
authors.initials: B
authors.lastname: Stengel
authors.forename: Philippe
authors.initials: P
authors.lastname: Guardiola
authors.forename: Stéphane
authors.initials: S
authors.lastname: Laurent
authors.forename: Pierre
authors.initials: P
authors.lastname: Boutouyrie
authors.forename: Marie
authors.initials: M
authors.lastname: Briet
mesh_terms: D000328:Adult; D000368:Aged; D001794:Blood Pressure / Q000502:physiology; D002318:Cardiovascular Diseases / Q000150:complications / Q000401:mortality / Q000503:physiopathology*; D002340:Carotid Artery Diseases / Q000150:complications / Q000401:mortality / Q000503:physiopathology*; D059168:Carotid Intima-Media Thickness; D005260:Female; D005919:Glomerular Filtration Rate / Q000502:physiology; D006801:Humans; D008297:Male; D008875:Middle Aged; D011379:Prognosis; D051436:Renal Insufficiency, Chronic / Q000150:complications / Q000401:mortality / Q000503:physiopathology*; D015996:Survival Rate; D059289:Vascular Stiffness / Q000502:physiology*