Markers of inflammation predict the long-term risk of developing chronic kidney disease: A population-based cohort study

Anoop Shankar, Liping Sun, Barbara E.K. Klein, Kristine E. Lee, Paul Muntner, F. Javier Nieto, Michael Y. Tsai, Karen J. Cruickshanks, Carla R. Schubert, Peter C. Brazy, Josef Coresh, Ronald Klein

Research output: Contribution to journalArticlepeer-review

119 Scopus citations

Abstract

In animal models, inflammatory processes have been shown to have an important role in the development of kidney disease. In humans, however, the independent relation between markers of inflammation and the risk of chronic kidney disease (CKD) is not known. To clarify this, we examined the relationship of several inflammatory biomarker levels (high-sensitivity C-reactive protein, tumor necrosis factor-α receptor 2, white blood cell count, and interleukin-6) with the risk of developing CKD in a population-based cohort of up to 4926 patients with 15 years of follow-up. In cross-sectional analyses, we found that all these inflammation markers were positively associated with the outcome of interest, prevalent CKD. However, in longitudinal analyses examining the risk of developing incident CKD among those who were CKD-free at baseline, only tumor necrosis factor-α receptor 2, white blood cell count, and interleukin-6 levels (hazard ratios comparing highest with the lowest tertile of 2.10, 1.90, and 1.45, respectively), and not C-reactive protein (hazard ratio 1.09), were positively associated with incident CKD. Thus, elevations of most markers of inflammation predict the risk of developing CKD. Each marker should be independently verified.

Original languageEnglish (US)
Pages (from-to)1231-1238
Number of pages8
JournalKidney international
Volume80
Issue number11
DOIs
StatePublished - Dec 2011

Bibliographical note

Funding Information:
This study was supported by the National Institutes of Health grant EYO6594 (RK, BEK), NIA grant AG11099 (KJC), NIDDK grant DK73217 (RK, AS), a grant from the American Heart Association (AS), and NIEHS grant 5-R03ES0018888-02 (AS).

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