Background The clinical utility of serum κ and λ free light chains (FLC) for the diagnosis and prognosis of plasma cell proliferative disorders is well established. We assessed the analytical performance of the N Latex FLC assays and compared it with the Freelite™ assays. Methods Analytical precision was assessed according to the CLSI EP5-A2 protocol. Method comparison was performed with 116 clinical samples and linearity was assessed on samples with monoclonal and polyclonal elevations of FLC. Analytical bias and variance was measured with two lots of N Latex FLC reagent. Results The N Latex FLC κ and λ assays had a total coefficient of variation of 5–7% across the analytical range. The slopes were 1.36 and 1.37 and the between-method variances were 40.0% and 45.4%, respectively, compared with the Freelite™. Good agreement in classification was observed for κ, λ and the κ/λ ratio (Cohen's κ 0.84, 0.76 and 0.89). Statistical non-linearity occurred commonly, but clinically significant non-linearity was observed in only one instance. Between-reagent lot variation was 7.3% and 10% for κ and λ, respectively. Conclusions The N Latex FLC assay has good precision, did not exhibit gross antigen excess and can be used in clinical practice based on the analytical performance characteristics.

BACKGROUND: It is important that cardiac troponin be measured accurately with a robust method to limit false results with potentially adverse clinical outcomes. In this study, we characterized the robustness of 4 analytical platforms by measuring the outlier rate between duplicate results. METHODS: We measured cardiac troponin concurrently in duplicate with 4 analyzers on 2391 samples. The outliers were detected from the difference between duplicate results and by calculating a z value: z = (result 1 − result 2) ÷ √(SD1_est² + SD2_est²), with z > 3.48 identifying outliers with a probability of 0.0005. RESULTS: The outlier rates were as follows: Abbott Architect i2000SR STAT Troponin-I, 0.10% (0.01%–0.19%); Beckman Coulter Access2 Enhanced AccuTnI, 0.44% (0.25%–0.63%); Roche Cobas e601 TroponinT hs, 0.06% (0.00%–0.13%); and Siemens ADVIA Centaur XP TnI-Ultra, 0.10% (0.01%–0.19%). The occurrence of outliers was higher than statistically expected on all platforms except the Cobas e601 (χ² = 2.7; P = 0.10). A conservative approach with a constant 10% CV and z > 5.0 identified outliers with clear clinical impact and resulted in outlier rates of 0.11% (0.02%–0.20%) with the Architect i2000SR STAT Troponin-I, 0.36% (0.19%–0.53%) with the Access2 Enhanced AccuTnI, 0.02% (0.00%–0.06%) with the Cobas e601 TroponinT hs, and 0.06% (0.00%–0.13%) with the ADVIA Centaur XP TnI-Ultra. CONCLUSIONS: Outliers occurred on all analytical platforms, at different rates. Clinicians should be made aware by their laboratory colleagues of the existence of outliers and the rate at which they occur.

BACKGROUND: Data to standardize and harmonize the differences between cardiac troponin assays are needed to support their universal status in diagnosis of myocardial infarction. We characterized the variation between methods, the comparability of the 99th-percentile cutoff thresholds, and the occurrence of outliers in 4 cardiac troponin assays. METHODS: Cardiac troponin was measured in duplicate in 2358 patient samples on 4 platforms: Abbott Architect i2000SR, Beckman Coulter Access2, Roche Cobas e601, and Siemens ADVIA Centaur XP. RESULTS: The observed total variances between the 3 cardiac troponin I (cTnI) methods and between the cTnI and cardiac troponin T (cTnT) methods were larger than expected from the analytical imprecision (3.0%–3.7%). The between-method variations of 26% between cTnI assays and 127% between cTnI and cTnT assays were the dominant contributors to total variances. The misclassification of results according to the 99th percentile was 3%–4% between cTnI assays and 15%–17% between cTnI and cTnT. The Roche cTnT assay identified 49% more samples as positive than the Abbott cTnI. Outliers between methods were detected in 1 patient (0.06%) with Abbott, 8 (0.45%) with Beckman Coulter, 10 (0.56%) with Roche, and 3 (0.17%) with Siemens. CONCLUSIONS: The universal definition of myocardial infarction should not depend on the choice of analyte or analyzer, and the between- and within-method differences described here need to be considered in the application of cardiac troponin in this respect. The variation between methods that cannot be explained by analytical imprecision and the discordant classification of results according to the respective 99th percentiles should be addressed.