Abstract
Background Patients with chronic kidney disease often have increased plasma cardiac troponin concentration in the absence of myocardial infarction. Incidence of myocardial infarction is high in this population, and diagnosis, particularly of non ST-segment elevation myocardial infarction (NSTEMI), is challenging. Knowledge of biological variation aids understanding of serial cardiac troponin measurements and could improve interpretation in clinical practice. The National Academy of Clinical Biochemistry (NACB) recommended the use of a 20% reference change value in patients with kidney failure. The aim of this study was to calculate the biological variation of cardiac troponin I and cardiac troponin T in patients with moderate chronic kidney disease (glomerular filtration rate [GFR] 30–59 mL/min/1.73 m2). Methods and results Plasma samples were obtained from 20 patients (median GFR 43.0 mL/min/1.73 m2) once a week for four consecutive weeks. Cardiac troponin I (Abbott ARCHITECT® i2000SR, median 4.3 ng/L, upper 99th percentile of reference population 26.2 ng/L) and cardiac troponin T (Roche Cobas® e601, median 11.8 ng/L, upper 99th percentile of reference population 14 ng/L) were measured in duplicate using high-sensitivity assays. After outlier removal and log transformation, 18 patients’ data were subject to ANOVA, and within-subject (CVI), between-subject (CVG) and analytical (CVA) variation calculated. Variation for cardiac troponin I was 15.0%, 105.6%, 8.3%, respectively, and for cardiac troponin T 7.4%, 78.4%, 3.1%, respectively. Reference change values for increasing and decreasing troponin concentrations were +60%/–38% for cardiac troponin I and +25%/–20% for cardiac troponin T. Conclusions The observed reference change value for cardiac troponin T is broadly compatible with the NACB recommendation, but for cardiac troponin I, larger changes are required to define significant change. The incorporation of separate RCVs for cardiac troponin I and cardiac troponin T, and separate RCVs for rising and falling concentrations of cardiac troponin, should be considered when developing guidance for interpretation of sequential cardiac troponin measurements.
Highlights
Chronic kidney disease (CKD) is common: 4.5% of the UK population have a glomerular filtration rate (GFR) below 60 mL/min/1.73 m2.1 The majority of individuals with chronic kidney disease (CKD) have moderate disease (CKD category G3) defined by a GFR of 30 to 59 mL/min/1.73 m2
There is a literature describing the biological variation of cardiac troponins in patients with kidney failure treated by dialysis but, to the best of our knowledge, this is the first study to report the biological variation of both cardiac troponin I (cTnI) and cardiac troponin T (cTnT) measured using high-sensitivity assays in patients with moderate CKD
The estimates of within-subject biological variation for cardiac troponin reported in the present study are similar to those previously reported in patients undergoing haemodialysis
Summary
Chronic kidney disease (CKD) is common: 4.5% of the UK population have a glomerular filtration rate (GFR) below 60 mL/min/1.73 m2.1 The majority of individuals with CKD have moderate disease (CKD category G3) defined by a GFR of 30 to 59 mL/min/1.73 m2. Diagnosis of acute myocardial infarction requires: (a) evidence of myocardial injury by observing at least one measure of cardiac troponin concentration exceeding the upper 99th percentile of a healthy reference population; (b) confirmation that such injury is acute, through observing a rise and/or fall of cardiac troponin concentration and; (c) evidence of myocardial ischaemia as demonstrated by accompanying characteristic symptoms and signs of myocardial infarction (e.g. electrocardiogram changes).[9] Patients with CKD are frequently observed to have concentrations of cardiac troponin that exceed the 99th percentile in the absence of myocardial infarction.[9,10,11,12] The increased plasma troponin concentration observed in CKD is most likely a reflection of the multifaceted burden of cardiovascular disease and creates a significant diagnostic problem.[9,10,13,14,15] The diagnosis of myocardial infarction in patients with CKD can be further complicated by absence of ischaemic symptoms and characteristic electrocardiogram changes.[13,16,17,18] In this situation, observation of changing cardiac troponin concentration over time is a useful pointer towards myocardial infarction, acute volume overload or heart failure may cause this pattern.[9]
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