P333 - PREOPERATIVE BASELINE TROPONIN AS A PREDICTOR OF MAJOR ADVERSE CARDIAC EVENTS FOLLOWING KIDNEY TRANSPLANTATION IN PATIENTS WITH END-STAGE KIDNEY DISEASE

Background: Cardiac troponins are frequently elevated following 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. 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 kidney transplant (KT). Our study aims to evaluate the association between pre-transplant baseline troponin levels and MACE in the year following KT.

METHODS AND RESULTS: This is a retrospective cohort study at a tertiary care center, consisting of 261 ESKD patients with cardiovascular disease referred for 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, or cardiac arrest. Patients undergoing multi-organ transplantation or lacking baseline troponin measurements were excluded. 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, 24 patients (18%) experienced MACE within a year of KT. Elevated baseline troponin levels, defined as exceeding the 99th percentile upper reference limit, were present in 93 patients (68%), while 43 (32%) had non-elevated troponin levels. Pre-KT demographics and comorbidities were comparable between the two groups. MACE post-KT was more prevalent in patients with elevated baseline troponin (22.6% vs. 7.0%, p=0.026). Additionally, among those who developed MACE, baseline troponin levels were markedly greater (4.2 times vs. 3.2 times the upper reference limit, p=0.048). Elevated troponin was associated with a nearly fourfold increased risk of MACE within one year of KT (OR 3.9; 95% CI: 1.1–13.8; p=0.036).

Conclusion: Among ESKD patients with cardiovascular disease, elevated baseline troponins were predictive of MACE in the year following KT. Further evaluation with long-term studies and larger cohorts remain necessary to validate the clinical utility of baseline troponin levels in risk-stratifying ESKD patients for adverse outcomes such as MACE following KT.