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Predictors of high sensitivity cardiac troponin T in chronic kidney disease patients: a cross-sectional study in the chronic renal insufficiency cohort (CRIC)

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posted on 2016-04-11, 00:00 authored by Ruth F. Dubin, Yongmei Li, Jiang He, Bernard G. Jaar, Radhakrishna Kallem, James P. Lash, Gail Makos, Sylvia E. Rosas, Elsayed Z. Soliman, Ray R. Townsend, Wei Yang, Alan S. Go, Martin Keane, Christopher deFilippi, Rakesh Mishra, Myles Wolf, Michael G. Shlipak
Background Cardiac troponin T is independently associated with cardiovascular events and mortality in patients with chronic kidney disease (CKD). Serum levels of high sensitivity cardiac troponin T (hs-TnT) reflect subclinical myocardial injury in ambulatory patients. We sought to determine the distribution and predictors of hs-TnT in CKD patients without overt cardiovascular disease (CVD). Methods We studied 2464 participants within the multi-ethnic Chronic Renal Insufficiency Cohort (CRIC) who did not have self-reported CVD. We considered renal and non-renal factors as potential determinants of hs-TnT, including demographics, comorbidities, left ventricular (LV) mass, serologic factors, estimated glomerular filtration rate (eGFR) and albumin to creatinine ratio. Results Hs-TnT was detectable in 81% of subjects, and the median (IQR) hs-TnT was 9.4 pg/ml (4.3-18.3). Analysis was performed using Tobit regression, adjusting for renal and non-renal factors. After adjustment, lower eGFR was associated with higher expected hs-TnT; participants with eGFR < 30 ml/min/1.73 m2 had 3-fold higher expected hs-TnT compared to subjects with eGFR > 60. Older age, male gender, black race, LV mass, diabetes and higher blood pressure all had strong, independent associations with higher expected hs-TnT. Conclusions Knowledge of the determinants of hs-TnT in this cohort may guide further research on the pathology of heart disease in patients with CKD and help to stratify sub-groups of CKD patients at higher cardiovascular risk.

Funding

We are indebted to the CRIC Study Investigators who are listed as authors, as well as the following CRIC Study Investigators: Lawrence J. Appel, MD, MPH, Harold I. Feldman, MD, MSCE, John W. Kusek, PhD, Akinlolu Ojo, MD, PhD, and Mahboob Rahman, MD. Support Funding for the CRIC Study was obtained under a cooperative agreement from National Institute of Diabetes and Digestive and Kidney Diseases (U01DK060990, U01DK060984, U01DK061022, U01DK061021, U01DK061028, U01DK060980, U01DK060963, and U01DK060902). This project was supported by M.S.’s R01 DK066488 award (principal investigator M.S.). R.D.is supported by K23 DK092354. In addition, this work was supported in part by: the University of Pennsylvania CTRC CTSA UL1 RR-024134, Johns Hopkins University UL1 RR-025005, University of Maryland GCRC M01 RR-16500, Clinical and Translational Science Collaborative of Cleveland, UL1TR000439 from the National Center for Advancing Translational Sciences (NCATS) component of the National Institutes of Health and NIH roadmap for Medical Research, Michigan Institute for Clinical and Health Research (MICHR) UL1RR024986, University of Illinois at Chicago CTSA UL1RR029879, Tulane University Translational Research in Hypertension and Renal Biology P30GM103337, Kaiser Permanente Northern California NIH/NCRR UCSF-CTSI UL1 RR-024131.

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Publisher Statement

© Dubin et al.; licensee BioMed Central Ltd. 2013 This article is published under license to BioMed Central Ltd. This is an open access article distributed under the terms of the Creative Commons Attribution License (http://​creativecommons.​org/​licenses/​by/​2.​0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

Publisher

BioMed Central

Language

  • en_US

issn

1471-2369

Issue date

2013-10-01

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