TY - JOUR
T1 - Fibroblast growth factor 23, high-sensitivity cardiac troponin, and left ventricular hypertrophy in CKD
AU - Smith, Kelsey
AU - Defilippi, Christopher
AU - Isakova, Tamara
AU - Gutiérrez, Orlando M.
AU - Laliberte, Karen
AU - Seliger, Stephen
AU - Kelley, Walter
AU - Duh, Show Hong
AU - Hise, Michael
AU - Christenson, Robert
AU - Wolf, Myles
AU - Januzzi, James
N1 - Funding Information:
Support: Funding for the main study in patients with CKD was provided by an investigator-initiated grant from Dade Behring (now Siemens Healthcare Diagnostics) to Dr deFilippi. For the present study, all hypotheses and analyses were generated and tested by the authors independently of industry support. This study was supported by the American Society of Nephrology Student Scholars Grant (to Ms Smith) and by grants from the National Institutes of Health ( K30RR02229207 , M01RR01066 , Mallinckrodt General Clinical Research Center at Massachusetts General Hospital ; and R01DK076116 to Dr Wolf).
PY - 2013/1
Y1 - 2013/1
N2 - Background: Detectable levels of cardiac troponins are common in individuals with chronic kidney disease (CKD), even in the absence of symptomatic cardiovascular disease. Abnormal cardiac troponin values are associated with coronary artery disease and left ventricular hypertrophy (LVH) and predict poor clinical outcomes. Elevated levels of fibroblast growth factor 23 (FGF-23) contribute to LVH in CKD. We investigated the association of FGF-23 and hs-cTnI (high-sensitivity cardiac troponin I) and hs-cTnT (high-sensitivity cardiac troponin T) levels in CKD and examined the role of LVH in this association. Study Design: Cross-sectional observational study. Setting & Participants: 153 stable outpatients with non-dialysis-dependent CKD. Predictor: The primary predictor was FGF-23 level. Outcomes: hs-cTnI, hs-cTnT. Measurements: FGF-23, hs-cTnI, hs-cTnT; left ventricular mass index (LVMI) assessed by echocardiography; coronary artery calcification (CAC) measured by computed tomography. LVMI and CAC were evaluated as potential mediators of the effect of FGF-23 on hs-cTnI/T. Results: Mean age was 64 ± 12 (SD) years, mean estimated glomerular filtration rate was 34 ± 11 mL/min/1.73 m 2, median FGF-23 level was 120 (25th-75th percentile, 79-223) reference unit (RU)/mL, median hs-cTnI level was 6.5 (25th-75th percentile, 3.5-14.5) pg/mL, and median hs-cTnT level was 16.8 (25th-75th percentile, 11.1-33.9) pg/mL. cTnI and cTnT concentrations were higher than the 99th percentile of a healthy population in 42% and 61% of patients, respectively. In unadjusted and multivariable-adjusted analyses, hs-cTnI/T levels were associated significantly with FGF-23 levels. Adjusting for LVMI, but not CAC, weakened the association of FGF-23 and hs-cTnI/T levels. Limitations: Vitamin D levels were not measured. The prevalence of coronary artery disease may have been underestimated because it was ascertained by self-report. Conclusions: Minimally elevated cTnI and cTnT levels, detectable by high-sensitivity assays, are associated with elevated FGF-23 levels in stable outpatients with CKD. FGF-23-associated LVH may contribute to detectable hs-cTnI/T levels observed in non-dialysis-dependent patients with CKD.
AB - Background: Detectable levels of cardiac troponins are common in individuals with chronic kidney disease (CKD), even in the absence of symptomatic cardiovascular disease. Abnormal cardiac troponin values are associated with coronary artery disease and left ventricular hypertrophy (LVH) and predict poor clinical outcomes. Elevated levels of fibroblast growth factor 23 (FGF-23) contribute to LVH in CKD. We investigated the association of FGF-23 and hs-cTnI (high-sensitivity cardiac troponin I) and hs-cTnT (high-sensitivity cardiac troponin T) levels in CKD and examined the role of LVH in this association. Study Design: Cross-sectional observational study. Setting & Participants: 153 stable outpatients with non-dialysis-dependent CKD. Predictor: The primary predictor was FGF-23 level. Outcomes: hs-cTnI, hs-cTnT. Measurements: FGF-23, hs-cTnI, hs-cTnT; left ventricular mass index (LVMI) assessed by echocardiography; coronary artery calcification (CAC) measured by computed tomography. LVMI and CAC were evaluated as potential mediators of the effect of FGF-23 on hs-cTnI/T. Results: Mean age was 64 ± 12 (SD) years, mean estimated glomerular filtration rate was 34 ± 11 mL/min/1.73 m 2, median FGF-23 level was 120 (25th-75th percentile, 79-223) reference unit (RU)/mL, median hs-cTnI level was 6.5 (25th-75th percentile, 3.5-14.5) pg/mL, and median hs-cTnT level was 16.8 (25th-75th percentile, 11.1-33.9) pg/mL. cTnI and cTnT concentrations were higher than the 99th percentile of a healthy population in 42% and 61% of patients, respectively. In unadjusted and multivariable-adjusted analyses, hs-cTnI/T levels were associated significantly with FGF-23 levels. Adjusting for LVMI, but not CAC, weakened the association of FGF-23 and hs-cTnI/T levels. Limitations: Vitamin D levels were not measured. The prevalence of coronary artery disease may have been underestimated because it was ascertained by self-report. Conclusions: Minimally elevated cTnI and cTnT levels, detectable by high-sensitivity assays, are associated with elevated FGF-23 levels in stable outpatients with CKD. FGF-23-associated LVH may contribute to detectable hs-cTnI/T levels observed in non-dialysis-dependent patients with CKD.
KW - Fibroblast growth factor 23
KW - chronic kidney disease
KW - high-sensitivity cardiac troponin
KW - left ventricular hypertrophy
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U2 - 10.1053/j.ajkd.2012.06.022
DO - 10.1053/j.ajkd.2012.06.022
M3 - Article
C2 - 22883134
AN - SCOPUS:84871236512
VL - 61
SP - 67
EP - 73
JO - American Journal of Kidney Diseases
JF - American Journal of Kidney Diseases
SN - 0272-6386
IS - 1
ER -
