Skip to main page content
U.S. flag

An official website of the United States government

Dot gov

The .gov means it’s official.
Federal government websites often end in .gov or .mil. Before sharing sensitive information, make sure you’re on a federal government site.

Https

The site is secure.
The https:// ensures that you are connecting to the official website and that any information you provide is encrypted and transmitted securely.

Access keys NCBI Homepage MyNCBI Homepage Main Content Main Navigation
. 2012 May;2(2):117-124.
doi: 10.1159/000337082. Epub 2012 Mar 20.

Chronic Inflammation and Coronary Atherosclerosis in Patients with End-Stage Renal Disease

Affiliations

Chronic Inflammation and Coronary Atherosclerosis in Patients with End-Stage Renal Disease

Maen B Nusair et al. Cardiorenal Med. 2012 May.

Abstract

The key role of chronic inflammation in the pathogenesis of atherosclerosis has become increasingly apparent in recent years based on the results of experimental, epidemiologic and clinical studies. Coronary artery disease and its complications occur with disproportionately high frequency in patients with end-stage renal disease (ESRD) and contribute substantially to cardiovascular morbidity and mortality in this population. Traditional cardiovascular risk factors occur commonly in patients with ESRD. In addition, a variety of patient-related and dialysis-related factors unique to ESRD predispose to chronic inflammation and by doing so are thought to contribute to coronary atherosclerosis and its complications. These risk factors may serve as therapeutic targets and as such may offer the potential for altering the natural history of coronary atherosclerosis in ESRD.

PubMed Disclaimer

Figures

Fig. 1
Fig. 1
Mechanisms by which traditional cardiovascular risk factors combine with risk factors for chronic inflammation to lead to accelerated atherosclerosis. Traditional cardiovascular risk factors combine with uremia and dialysis-related risk factors to cause endothelial dysfunction and pro-inflammatory cytokine release. This stimulates production of acute phase reactants (CRP, serum amyloid A, fibrinogen) ultimately leading to accelerated atherosclerosis.

Similar articles

Cited by

References

    1. Leitinger N. Oxidized phospholipids as modulators of inflammation in atherosclerosis. Curr Opin Lipidol. 2003;14:421–430. - PubMed
    1. Dai G, Kaazempur-Mofrad MR, Natarajan S, Zhang Y, Vaughn S, Blackman BR, Kamm RD, Garcia-Cardena G, Gimbrone MA., Jr Distinct endothelial phenotypes evoked by arterial waveforms derived from atherosclerosis-susceptible and resistant regions of human vasculature. Proc Natl Acad Sci USA. 2004;101:14871–14876. - PMC - PubMed
    1. Cybulsky MI, Iiyama K, Li H, Zhu S, Chen M, Iiyama M, Davis V, Gutierrez-Ramos JC, Connelly PW, Milstone DS. A major role for VCAM-1, but not ICAM-1, in early atherosclerosis. J Clin Invest. 2001;107:1255–1262. - PMC - PubMed
    1. Cybulsky MI, Gimbrone MA., Jr Endothelial expression of a mononuclear leukocyte adhesion molecule during atherogenesis. Science. 1991;251:788–791. - PubMed
    1. Boring L, Gosling J, Cleary M, Charo IF. Decreased lesion formation in CCR2-/- mice reveals a role for chemokines in the initiation of atherosclerosis. Nature. 1998;394:894–897. - PubMed

LinkOut - more resources