Terminal renal failure as a contributor to high-sensitivity cardiac troponin T elevations: insights from patients undergoing renal transplantation.

Abstract

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. 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. 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). 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.