Association of troponin-defined myocardial injury with adverse long-term survival among patients with chronic kidney disease

OBJECTIVE: Chronic kidney disease (CKD) is associated with increased mortality, however, the impact of troponin-defined myocardial injury within this population remains poorly understood. This study aimed to investigate the associations between troponin-defined myocardial injury and long-term mortality in CKD patients. METHODS: This observational study analyzed 22,772,953 weighted records of adult CKD patients from National Health and Nutrition Examination Survey (1999-2004) databases. Myocardial injury was defined by at least one elevated high-sensitivity troponin (hs-cTn) assay, present in 26.6% of the cohort. Cox regression models adjusted for baseline characteristics and comorbidities were used to assess the associations between troponin-defined myocardial injury and all-cause and cardiovascular mortality. Sensitivity analyses excluding patients with known cardiovascular disease (CVD) were performed to evaluate the robustness of the findings. RESULTS: Patients with troponin-defined myocardial injury were older and had a higher prevalence of CVD, hypertension, diabetes, as well as a lower estimated glomerular filtration rate (eGFR), compared with those without troponin-defined myocardial injury. Over a median follow-up of 11.6 years, survival was significantly worse among patients with troponin-defined myocardial injury at 1, 5, 10, and 15 years. The adjusted hazard ratios (aHR) for all-cause mortality and cardiovascular mortality in patients with troponin-defined myocardial injury were 1.81 (95% CI 1.51-2.17) and 2.03 (95% CI 1.47-2.79), respectively. Sensitivity analysis excluding records with pre-existing CVD showed similar trends, with an aHR of 1.86 (95% CI 1.56-2.21) for all-cause mortality and 2.44 (95% CI 1.83-3.24) for cardiovascular mortality. CONCLUSION: As a marker for troponin-defined myocardial injury, hs-cTns were independently associated with worse long-term survival among CKD patients. However, the observational design precludes causal inference, and single time-point troponin measurements limit the assessment of dynamic changes in myocardial injury.