Associations Between Cardiac Biomarkers and Cardiac Structure and Function in CKD
JournalKidney International Reports
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AbstractIntroduction: Subclinical changes to cardiac structure and function detected with echocardiography precede the development of clinical heart failure (HF) in persons with chronic kidney disease (CKD). Circulating cardiac biomarkers may reflect these pathophysiological changes. This study investigated associations between established biomarkers (N-terminal pro-B-type natriuretic peptide [NT-proBNP] and high-sensitivity troponin T [hsTnT]) and novel biomarkers (growth differentiation factor 15 [GDF-15], galectin-3 [Gal-3], and soluble ST-2 [sST-2]), using echocardiographic measurements in persons with CKD. Methods: In cross-sectional analyses among 2101 participants with mild to moderate CKD in the Chronic Renal Insufficiency Cohort (CRIC), biomarker levels measured at baseline were evaluated with echocardiographic measurements 1 year later. These included left ventricular mass index (LVMI), left ventricular end-systolic volume (LVESV), left ventricular end-diastolic volume (LVEDV), left ventricular ejection fraction (LVEF), and left atrial diameter (LAD). Multivariable linear regression analyses tested associations of each biomarker with echocardiographic measurements, adjusting for covariates. Results: GDF-15 was significantly associated with higher LVMI (1.0 g/m2.7; 95% CI, 0.4-1.7), LVESV (0.4 ml/m2.7; 95% CI, 0.0-0.7), and LVEDV (0.6 ml/m2.7; 95% CI, 0.1-1.1), but not with LVEF or LAD. These findings were not significant when adjusting for NT-proBNP and hsTnT. Gal-3 and sST-2 had no significant associations. Higher levels of NT-proBNP and hsTnT were associated with all echocardiographic measurements. Conclusion: In patients with CKD, the novel biomarker GDF-15, a marker of inflammation and tissue injury, and clinical biomarkers NT-proBNP and hsTnT, were associated with echocardiographic measurements of subclinical cardiovascular disease. Collectively, these biomarkers may highlight biological pathways that contribute to the development of clinical HF.
SponsorsThis study was supported by R01 DK103612 (to NB) and R01 01DK104730 (to AHA). Roche Diagnostics provided partial funding for the NT-proBNP and hsTnT assays. 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 ). In addition, this work was supported in part by the Perelman School of Medicine at the University of Pennsylvania Clinical and Translational Science Award NIH/NCATS UL1TR000003; Johns Hopkins University UL1 TR-000424 ; the University of Maryland GCRC M01 RR-16500 ; the 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; the Michigan Institute for Clinical and Health Research (MICHR) UL1TR000433 , the University of Illinois at Chicago CTSA UL1RR029879 ; Tulane COBRE for Clinical and Translational Research in Cardiometabolic Diseases P20 GM109036; and Kaiser Permanente NIH/NCRR UCSF-CTSI UL1 RR-024131.
chronic renal insufficiency
growth differentiation factor 15
Identifier to cite or link to this itemhttps://www.scopus.com/inward/record.uri?eid=2-s2.0-85086582436&doi=10.1016%2fj.ekir.2020.04.031&partnerID=40&md5=8b7861cd26bdf579dfbe708fe4a0be38; http://hdl.handle.net/10713/13209