Abstract

Introduction: Measurement of the biological variation of cardiac troponin (cTn) allows determination of reference change values (RCVs) to use for interpreting serial testing. Using plasma collected serially over 12-months from a stable outpatient hemodialysis (HD) population, our goals were two-fold. First, we calculated RCVs for hs-cTnI and hs-cTnT assays. Second, we determined outcomes based on hs-cTnI and hs-cTnT RCVs. Methods: hs-cTnI (Abbott) and hs-cTnT (Roche) were measured in 677 stable outpatient HD patients (enrolled May 2011-November 2012). Hazard ratios (HR), based on RCVs calculated for each hs-cTn assay, for ‘all-cause’, ‘sudden cardiac death (SCD)’ and ‘infectious’ mortality were determined with serial measurements obtained 3 months apart. Results: Patient demographics were: mean age 59±14y; mean dialysis duration 5.2±4.2y; 53% male; 59% African American and 50% diabetic ESRD. 18.6% of patients died during a 3-year follow-up. RCVs were: hs-cTnI, +37% and -30%; hs-cTnT, +25% and -20%. Patients with serial hs-cTnI and hs-cTnT changes >RCV had all-cause mortality of 25.2% and 23.8% respectively, compared to 15.0% and 16.5% with ≤RCV (both p<0.05). Outcomes and adjusted HRs are shown in Table. Patients with serial hs-cTnI and hs-cTnT changes >RCV showed a greater risk of all-cause mortality compared to ≤RCV (HR: 1.9 (95% CI: 1.4, 2.8), p=0.0003; and HR: 1.7 (95% CI: 1.2, 2.4), p=0.0066; respectively). However, only hs-cTnI changes >RCV were predictive of SCD (HR: 2.6 (95% CI: 1.3, 5.1), p=0.005). Conclusions: Our findings are unique in two ways. First we determined the biological variation of hs-cTnI and hs-cTnT in a large HD population. Second, based on the RCV for each hs-assay, serial changes in hs-cTnI and hs-cTnT >RCV identify patients at greater risk of all-cause mortality, with hs-cTnI also predictive of SCD. These findings support the use of serial changes >RCV for risk-stratification in HD patients.

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