Preoperative baseline troponin as a predictor of major adverse cardiac events following kidney transplantation in patients with end-stage kidney disease

Abstract Introduction Cardiac biomarkers, such as troponins, are indicators of myocardial ischemia. These biomarkers are frequently elevated after non-cardiac surgery, and clinically silent elevations have been associated with major adverse cardiac events (MACE). As such, many patients are evaluated for myocardial injury after non-cardiac surgery, defined as one or more postoperative troponin measurements exceeding the 99th percentile upper reference limit of the assay within 30 days of surgery. However, interpreting postoperative troponins in patients with end-stage kidney disease (ESKD) is challenging, as they often have elevated baseline troponin levels prior to surgery in the absence of myocardial ischemia. This is particularly relevant given that cardiovascular disease remains the leading cause of morbidity and mortality among kidney transplant (KT) recipients. Purpose To date, no studies have examined the utility of baseline troponin levels in patients with ESKD as a tool to risk stratify patients prior to KT. Our study aims to evaluate the association between pre-KT baseline troponin levels and the development of MACE in the year following KT. Methods This is a retrospective cohort study at a tertiary care center, consisting of 261 consecutive ESKD patients with cardiovascular disease referred for cardiac assessment prior to KT between January 2013 and January 2024. The primary endpoint was MACE in the year following KT, defined as all-cause death, non-fatal myocardial infarction, non-fatal stroke, coronary revascularization, heart failure hospitalization, and cardiac arrest. Patients undergoing multi-organ transplantation or lacking baseline troponin measurements were excluded. We performed descriptive statistics and logistic regression modelling to predict MACE. Results Of the 261 patients referred, 153 (59%) had a KT, 83 (32%) died pre-KT, and 25 (9%) were removed from the transplant program. Among the 153 patients who received a transplant, 136 met the inclusion criteria. Of these, 112 patients (82%) were free of MACE, while 24 (18%) experienced MACE within a year of KT. Patients who developed MACE were more likely to have elevated baseline troponin levels exceeding the 99th percentile upper reference limit (87.5% vs. 64.2%, p=0.026). Furthermore, those who developed MACE had greater baseline troponin elevations (4.2x upper reference limit vs. 3.2x upper reference limit, p=0.048). Baseline troponin levels above the 99th percentile upper reference limit were associated with a nearly fourfold increased likelihood of MACE in the year following KT (OR 3.9; 95% CI: 1.1–13.8; p=0.036). Conclusion Among ESKD patients with cardiovascular disease, elevated baseline troponin was predictive of MACE in year following KT. Further evaluation with long-term studies and larger cohorts are necessary to validate the clinical utility of baseline troponin levels in risk stratifying ESKD patients for adverse outcomes such as MACE following KT.

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