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. 2025 Dec;47(1):2440512.
doi: 10.1080/0886022X.2024.2440512. Epub 2024 Dec 18.

Elevated concentrations of cardiac troponin T are associated with thoracic aortic calcification in non-dialysis chronic kidney disease patients of stage G3 to G5

Wenjiao Zhu  1   2 , Zhiman Lai  3 , Miaorong Xue  1   2 , Shaozhen Feng  1   2 , Pinning Feng  4 , Xiantian Pan  5 , Xiaojie Ke  1   2 , Xionghui Chen  1   2 , Zhijian Li  1   2 , Haiping Mao  1   2 , Xiao Yang  1   2 , Fengxian Huang  1   2 , Wei Chen  1   2 , Yuanwen Xu  1   2 , Shurong Li  3 , Qunying Guo  1   2
Affiliations

Elevated concentrations of cardiac troponin T are associated with thoracic aortic calcification in non-dialysis chronic kidney disease patients of stage G3 to G5

Wenjiao Zhu et al. Ren Fail. 2025 Dec.

Abstract

Background: Vascular calcification (VC), especially coronary artery calcification (CAC), serves as a robust predictor of cardiovascular mortality in chronic kidney disease (CKD) patients. Recent studies have revealed that the presence of extra-coronary calcifications (ECCs) contributes to cardiovascular disease (CVD). Elevated myocardial injury markers predict mortality risk in CKD patients and are associated with CVD. Nevertheless, the relationship between VC, including CAC and ECCs, and myocardial injury markers remain unexplored in non-dialysis CKD patients.

Methods: In 278 non-dialysis CKD patients of stage G3 to G5, we assessed calcified scores in CAC (Agatston score) and ECCs including thoracic aortic calcification (TAC), abdominal aortic calcification (AAC), carotid artery calcification, and valvular calcification. We analyzed the relationships between VC and myocardial injury markers of cardiac troponin T (cTnT) and creatine kinase-MB (CK-MB).

Results: A total of 278 non-dialysis CKD patients (median age 52.4 ± 13.2; male 65.1%; diabetes 33.5%) were enrolled. A total of 71.8% (227) of patients had cTnT levels above the upper limit of normal (> 0.014 ng/mL). Moderate to severe (calcified score ≥100 vs. <100), CAC (OR 6.39; 95% CI 1.03-39.61) and TAC (OR 6.16; 95% CI 1.76-21.55) were significantly associated with higher cTnT concentrations after adjustment for confounders. Additionally, male sex and a lower eGFR were also associated with cTnT elevation. However, when we included CAC and TAC in one model, only moderate to severe TAC (OR 4.85; 95% CI 1.38-16.96) was a risk factor for cTnT elevation, but not CAC. Furthermore, patients with severer TAC presented lower diastolic blood pressure (DBP), wider pulse pressure (p < 0.001) and higher prevalence of left ventricular hypertrophy (LVH).

Conclusion: Moderate to severe thoracic aortic calcification (TAC score ≥ 100) is significantly associated with elevated cTnT concentrations in non-dialysis CKD patients of stage G3 to G5. The linkage may result from decreased coronary perfusion and relative myocardial ischemia.

Keywords: Coronary artery calcification; cardiac troponin T; chronic kidney disease; creatine kinase-MB; thoracic aortic calcification.

Plain language summary

Vascular calcification (VC), including coronary artery calcification (CAC) and extra-coronary calcifications (ECCs), is recognized as a strong predictor of cardiovascular mortality in patients with chronic kidney disease (CKD). In this study involving 278 non-dialysis CKD patients of stage G3 to G5, we assessed the calcification scores for CAC, thoracic aortic calcification (TAC), abdominal aortic calcification (AAC), carotid artery calcification, and valvular calcification. And explored relationship between VC and myocardial injury markers such as cardiac troponin T (cTnT) and creatine kinase-MB (CK-MB). The study found that cTnT levels were associated with the severity of CAC (OR 6.39; 95% CI 1.03-39.61) and TAC (OR 6.16; 95% CI 1.76-21.55). After adjusting for confounding factors, only moderate to severe TAC (OR 4.85; 95% CI 1.38-16.96) was identified as a significant risk factor for elevated cTnT levels, but not CAC. Furthermore, the potential association between TAC and myocardial ischemia may be due to decreased coronary perfusion and left ventricular hypertrophy (LVH). These findings underscore the importance of monitoring TAC which may be more effectively associated with cardiovascular risks.

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Conflict of interest statement

The authors report there are no competing interests to declare.

Figures

None
Graphical abstract
Figure 1.
Figure 1.
The distribution of cardiac troponin T (cTnT) and creatine kinase-MB (CK-MB) concentrations in CKD stage G3 to G5. Data are presented as median (IQR). Note: ** p < 0.05 NS: p > 0.05.
Figure 2.
Figure 2.
The distribution of cardiac troponin T (cTnT) and creatine kinase-MB (CK-MB) concentrations in different degree of severity of CAC and TAC. Data were presented as median (IQR).
Figure 3.
Figure 3.
Fully adjusted model (model 3) of CAC (coronary-artery calcification), TAC (thoracic aortic calcification) and CVC (cardiovascular calcification) for cTnT: adjusted for age, sex, BMI, diabetes, pulse pressure, smoking history, drinking history, coronary atherosclerosis history, eGFR (estimated glomerular filtration rate), NT-proBNP (N-terminal pro-b-type natriuretic peptide), serum albumin, 24-h urine protein, fibrinogen, iPTH (intact parathyroid hormone), serum phosphate, triglycerides, LDL-c (low density lipoprotein-cholesterol) and antihypertensive medicine.
Figure 4.
Figure 4.
Multivariate logistic regression analysis for cTnT concentrations with CAC and TAC. Note: Multivariate analysis: adjusted for model 3 and CAC and TAC. TAC: thoracic aortic calcification; CAC: coronary artery calcification; LDL-c: low density lipid -cholesterol; iPTH: intact parathyroid hormone; ALB: Albumin; eGFR: estimated glomerular filtration rate; BMI: body mass index.
Figure 5.
Figure 5.
The relationship between the severity of thoracic aortic calcification (TAC) and blood pressure. Note: TAC = thoracic aortic calcification; DBP = diastolic blood pressure.
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