Background
False cardiac troponin (cTn) elevations from non-cardiac causes are a major concern. We aimed to assess terminal renal failure as a possible non-cardiac cause of elevated high-sensitivity cTnT (hs-cTnT) concentrations using renal transplantation as an in vivo model of rapid restoration of renal function.
Methods
We analysed consecutive patients with end-stage renal disease (ESRD) undergoing renal transplantation at a single centre. Patients with perioperative myocardial infarction or injury were excluded. Changes in hs-cTnT and creatinine were measured pretransplant and at four post-transplant intervals (day 1, days 2–5 and days 14–180). A decrease of ≥25% in hs-cTnT within 24 hours post-transplant was deemed evidence of renal clearance recovery.
Results
Among 45 patients (median age 67 years, 31% women), the median pretransplant plasma creatinine concentration was 608 μmol/L (IQR 482–830), and fell to 425 μmol/L (IQR 337–619) on day 1, 289 μmol/L (IQR 201–492) on days 2–5 and 126 μmol/L (IQR 103–191) on days 14–180 (p<0.001, p<0.001 and p=0.003, respectively). The median pretransplant hs-cTnT concentration was 48 ng/L (IQR 34–70). It fell to 26 ng/L (IQR 15–38; geometric mean of relative change 36%) on day 1 (p<0.001) and then remained constant on days 2–5 (26 ng/L (IQR 18–35)) and days 14–180 (25 ng/L (IQR 20–30), p=ns).
Conclusion
Terminal renal failure is a non-cardiac cause of elevated circulating hs-cTnT concentrations, contributing more than one-third in this cohort, while the remaining two-thirds seem related to chronic cardiomyocyte injury.
