Impaired renal function can increase cardiac troponin levels due to reduced elimination, potentially affecting its diagnostic utility. Limited data exist on high-sensitivity cardiac troponin I (hs-cTnI) kinetics after cardiac surgery relative to renal function. This study evaluates how impaired renal function influences hs-cTnI kinetics following cardiac surgery, distinguishing between patients with and without postoperative myocardial infarction (PMI). We conducted a retrospective analysis of adult patients who underwent elective cardiac surgery at our hospital from January 2013 to May 2019. Serial hs-cTnI measurements were taken from baseline up to 48h post-surgery. Renal function was assessed using the MDRD formula, defining impaired renal function as a GFR < 60ml/min. Acute kidney injury (AKI) was based on postoperative creatinine levels, and PMI was defined by ARC-2 criteria. Predictors of long-term all-cause mortality were analyzed using Cox regression. Out of 14,355 patients (51.4% CABG, 39.4% valvular procedures, 9.2% thoracic aortic procedures), 139 (1.0%) had PMI. Hs-cTnI levels were higher in patients with impaired renal function across the cohort and in those without PMI. However, in patients with PMI, hs-cTnI levels did not vary significantly with renal function. Elevated hs-cTnI ≥ 213 times the upper limit of normal was a significant predictor of long-term mortality regardless of renal function (hazard ratio: 1.28, 95% CI: 1.17-1.40, p < 0.001), but early postoperative hs-cTnI measures held poor discriminatory yield to predict PMI with an AUC of 0.55 (95% confidence intervals: 0.54-0.56). Renal function and acute kidney injury affect hs-cTnI kinetics post-surgery only in patients without PMI. Elevated hs-cTnI remains a strong predictor of long-term mortality, independent of renal function, but early postoperative detection of PMI requires additional metrics, including ECG, transthoracic echocardiography (TTE), and signs of hemodynamic instability.
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