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Arterial aging and arterial disease: interplay between central hemodynamics, cardiac work, and organ flow—implications for CKD and cardiovascular disease

https://doi.org/10.1038/kisup.2011.5Get rights and content
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Cardiovascular disease is an important cause of morbidity and mortality in patients with chronic kidney disease (CKD) and end-stage renal disease (ESRD). All epidemiological studies have clearly shown that accelerated arterial and cardiac aging is characteristic of these populations. Arterial premature aging is heterogeneous. It principally involves the aorta and central capacitive arteries, and is characterized by preferential aortic stiffening and disappearance of stiffness/impedance gradients between the central and peripheral arteries. These changes have a double impact: on the heart, upstream, with left ventricular hypertrophy and decreased coronary perfusion; and, downstream, on renal and brain microcirculation (decrease in glomerular filtration and cognitive functions). Multifactorial at origin, the pathophysiology of aortic ‘progeria’ and microvascular disorders in CKD/ESRD is not well understood and should be the focus of interest in future studies.

Keywords

aging
arteriosclerosis
arterial stiffness
end-stage renal disease
pressure waves

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TO CITE THIS ARTICLE: London G, Covic A, Goldsmith D et al. Arterial aging and arterial disease: interplay between central hemodynamics, cardiac work, and organ flow—implications for CKD and cardiovascular disease. Kidney Int Sup 2011; 1: 10–12.

AC has received consulting fees from Abbott Laboratories and received lecture fees from F. Hoffmann-La Roche, Amgen, and Fresenius Medical Care Holdings. AM-C has received consulting fees from Abbott Laboratories, Roche Spain, and Abbott Spain. AO has received grant support from the Spanish Government. AW has received lecture fees from Amgen, F. Hoffmann-La Roche, and Janssen-Cileg. AW has also received grant support from Astellas Pharma. DF has received funding from the EU. DG has received consulting fees and lecture fees from Shire, Genzyme, Novartis AG, Sandoz, Pfizer, and Fresenius Medical Care Holdings. FWD has received funding from Amgen and Baxter. GL has received consulting fees from Amgen and Sandoz. GL has also received lecture fees from Amgen, Sandoz, Genzyme, and Shire. PJB has received consulting fees from Medtronic and has received grant support from Ardian and Novartis AG. RA has received consulting fees from Amgen, Abbott Laboratories, Merck, Affymax, Takeda Pharmaceutical Company, Daiichi Sankyo, Celgene, Watson Pharmaceuticals, and Rockwell Medical. RA has also received lecture fees from Abbott Laboratories, Merck, and Medscape. ZM has received lecture fees from Amgen, Shire, Genzyme, FMC, and Merck Sharp & Dohme. ZM has received grant support from Baxter, Amgen, FMC, Shire, and Genzyme. The remaining authors declared no competing interests.