Interpreting cardiac troponin results from high-sensitivity assays in chronic kidney disease without acute coronary syndrome.

Overview

abstract

BACKGROUND: Quantification and comparison of high-sensitivity (hs) cardiac troponin I (cTnI) and cTnT concentrations in chronic kidney disease (CKD) have not been reported. We examined the associations between hs cTnI and cTnT, cardiovascular disease, and renal function in outpatients with stable CKD. METHODS: Outpatients (n = 148; 16.9% with prior myocardial infarction or coronary revascularization) with an estimated glomerular filtration rate (eGFR) of <60 mL · min⁻¹ · (1.73 m²)⁻¹ had serum cTnI (99th percentile of a healthy population = 9.0 ng/L), and cTnT (99th percentile = 14 ng/L) measured with hs assays. Left ventricular ejection fraction (LVEF) and mass were assessed by echocardiography, and coronary artery calcification (CAC) was determined by computed tomography. Renal function was estimated by eGFR and urine albumin/creatinine ratio (UACR). RESULTS: The median (interquartile range) concentrations of cTnI and cTnT were 6.3 (3.4-14.4) ng/L and 17.0 (11.2-31.4) ng/L, respectively; 38% and 68% of patients had a cTnI and cTnT above the 99th percentile, respectively. The median CAC score was 80.8 (0.7-308.6), LV mass index was 85 (73-99) g/m², and LVEF was 58% (57%-61%). The prevalences of prior coronary disease events, CAC score, and LV mass index were higher with increasing concentrations from both hs cardiac troponin assays (P < 0.05 for all). After adjustment for demographics and risk factors, neither cardiac troponin assay was associated with CAC, but both remained associated with LV mass index as well as eGFR and UACR. CONCLUSIONS: Increased hs cTnI and cTnT concentrations are common in outpatients with stable CKD and are influenced by both underlying cardiac and renal disease.