| Literature DB >> 21493771 |
Marie Briet1, Cédric Collin, Alexandre Karras, Stéphane Laurent, Erwan Bozec, Christian Jacquot, Bénédicte Stengel, Pascal Houillier, Marc Froissart, Pierre Boutouyrie.
Abstract
In CKD, large arteries remodel and become increasingly stiff. The greater pulsatile pressure reaching the glomerulus as a result of increased aortic stiffness could induce renal damage, suggesting that the stiffening and remodeling of large arteries could affect the progression of CKD. We measured carotid-femoral pulse wave velocity, aortic pressure and carotid remodeling and stiffness parameters in 180 patients with CKD (mean measured GFR, 32 ml/min per 1.73 m(2)) and followed them prospectively for a mean of 3.1 years. During follow-up, carotid stiffness significantly increased (+0.28 ± 0.05 m/s; P<0.0001) but aortic stiffness did not. Carotid intima-media thickness decreased significantly during follow-up and the internal diameter of the carotid increased, producing increased circumferential wall stress (+2.08 ± 0.43 kPa/yr; P<0.0001). In a linear mixed model, circumferential wall stress significantly associated with faster GFR decline after adjustment for risk factors of cardiovascular disease and progression of CKD. In a multivariable Cox model, carotid circumferential wall stress and pulse pressure independently associated with higher risk for ESRD. None of the arterial stiffness parameters associated with progression of CKD. In conclusion, maladaptive remodeling of the carotid artery and increased pulse pressure independently associate with faster decline of renal function and progression to ESRD.Entities:
Mesh:
Year: 2011 PMID: 21493771 PMCID: PMC3083318 DOI: 10.1681/ASN.2010080863
Source DB: PubMed Journal: J Am Soc Nephrol ISSN: 1046-6673 Impact factor: 10.121