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Inflammation and Arterial Stiffness in Chronic Kidney Disease: Findings From the CRIC Study
Journal article   Open access   Peer reviewed

Inflammation and Arterial Stiffness in Chronic Kidney Disease: Findings From the CRIC Study

Eliot Peyster, Jing Chen, Harold I Feldman, Alan S Go, Jayanta Gupta, Nandita Mitra, Qiang Pan, Anna Porter, Mahboob Rahman, Dominic Raj, …
American journal of hypertension, Vol.30(4), pp.400-408
04-01-2017
PMCID: PMC5861572
PMID: 28391349

Abstract

Adult Aged Blood Pressure C-Reactive Protein - immunology Cohort Studies Enzyme-Linked Immunosorbent Assay Female Fibrinogen - immunology Follow-Up Studies Humans Inflammation - immunology Interleukin 1 Receptor Antagonist Protein - immunology Interleukin-1beta - immunology Interleukin-6 - immunology Linear Models Male Middle Aged Proteinuria - etiology Pulse Wave Analysis Renal Insufficiency, Chronic - complications Renal Insufficiency, Chronic - immunology Renal Insufficiency, Chronic - physiopathology Transforming Growth Factor beta - immunology Tumor Necrosis Factor-alpha - immunology Vascular Stiffness - immunology
Chronic kidney disease (CKD) and arterial stiffness are associated with increased cardiovascular morbidity and mortality. Inflammation is proposed to have a role in the development of arterial stiffness, and CKD is recognized as a proinflammatory state. Arterial stiffness is increased in CKD, and cross-sectional data has suggested a link between increased inflammatory markers in CKD and higher measures of arterial stiffness. However, no large scale investigations have examined the impact of inflammation on the progression of arterial stiffness in CKD. We performed baseline assessments of 5 inflammatory markers in 3,939 participants from the chronic renal insufficiency cohort (CRIC), along with serial measurements of arterial stiffness at 0, 2, and 4 years of follow-up. A total of 2,933 participants completed each of the follow-up stiffness measures. In cross-sectional analysis at enrollment, significant associations with at least 2 measures of stiffness were observed for fibrinogen, interleukin-6, high-sensitivity C-reactive protein, proteinuria, and composite inflammation score after adjustment for confounders. In longitudinal analyses, there were few meaningful correlations between baseline levels of inflammation and changes in metrics of arterial stiffness over time. In a large cohort of CKD participants, we observed multiple significant correlations between initial markers of inflammation and metrics of arterial stiffness, but baseline inflammation did not predict changes in arterial stiffness over time. While well-described biologic mechanisms provide the basis for our understanding of the cross-sectional results, continued efforts to design longitudinal studies are necessary to fully elucidate the relationship between chronic inflammation and arterial stiffening.
url
https://doi.org/10.1093/ajh/hpw164View
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