Performance of the microINR Point-of-Care System Used by Self-Testing Patients: A Multicenter Clinical Trial.

Introduction Anticoagulation monitoring is a major practical and clinical challenge. We assessed the performance of the microINR system in patient self-testing (PST). Methods This study was performed at four US medical centers. After the training visit of warfarin anticoagulated patients ( n = 117) on microINR system, PST was performed at home and in two visits to the medical centers. At the medical centers, both PST and healthcare professionals (HCPs) performed duplicate tests with the microINR System. A venous blood sample for the laboratory testing was also extracted. Accuracy and precision were assessed. Results The comparison between microINR PST results and microINR HCP results revealed an equivalence with a slope of 1.00 (95% confidence interval [CI]: 1.00-1.00), and an intercept of 0.00 (95% CI: 0.00-0.00). When compared with the laboratory analyzer, microINR PST results also showed good correlation with a slope of 0.94 (95% CI: 0.86-1.04) and an intercept of 0.14 (95% CI: -0.09-0.34). Predicted bias values at international normalized ratio (INR) 2.0, 3.5, and 4.5 were 0% against HCP and ≤2.5% against the laboratory. Analytical agreement with both HCP and laboratory was 100% according to ISO17593 and 99.1 and 100% according to CLSI POCT14 with HCP and laboratory, respectively. Clinical agreement with HCP regarding 2.0-4.0 as INR therapeutic range was 98% (within range). The precision (coefficient of variation) of microINR system used by PST was comparable to HCP. Conclusion The microINR results when used by self-testing patients show satisfactory concordance to both HCP results and laboratory analyzer. The microINR system is adequate for self-testing use.

Reference intervals of urinary acute kidney injury (AKI) markers [IGFBP7]∙[TIMP2] in apparently healthy subjects and chronic comorbid subjects without AKI.

BACKGROUND: Insulin-like growth factor-binding protein 7 (IGFBP7) and tissue inhibitor of metalloproteinases-2 (TIMP-2) have demonstrated significantly improved diagnostic performance in assessing risk for acute kidney injury (AKI) compared with existing biomarkers. We present the findings of a multi-site trial to determine the reference intervals for these biomarkers in apparently healthy adults and those with stable chronic morbid conditions without AKI. METHODS: A urine specimen was collected from apparently healthy subjects (N=378) and subjects with at least one stable chronic morbidity (N=372). Specimens were kept frozen until analysis with the NephroCheck® Test (Astute Medical). The test is comprised of fluorescence immunoassays for IGFBP7 and TIMP-2 and is used with the Astute140® Meter which quantifies the concentration of each biomarker. The meter multiplies the concentrations of IGFBP7 and TIMP-2 and displays the result as a numerical value ([IGFBP7]∙[TIMP-2]) expressed in (ng/ml)(2)/1000 which is called the AKIRisk™ Score. RESULTS: The reference intervals (inner 95%) for [IGFBP7]∙[TIMP-2] in all subjects (N=750), apparently healthy subjects, and subjects with stable chronic morbidities were 0.04-2.22, 0.04-2.25, and 0.05-2.20 (ng/ml)(2)/1000 respectively. There was no statistical difference between reference intervals for apparently healthy and chronic stable morbid cohorts (p=0.42). CONCLUSIONS: Our investigation showed that urine [IGFBP7]∙[TIMP-2] values were not elevated in patients with stable chronic morbidities who did not have AKI.

Demographic data for urinary Acute Kidney Injury (AKI) marker [IGFBP7]·[TIMP2] reference range determinations.

This data in brief describes characteristics of chronic stable comorbid patients who were included in reference range studies of [IGFBP7]·[TIMP-2] "Reference Intervals of Urinary Acute Kidney Injury (AKI) Markers [IGFBP7]·[TIMP2] in Apparently Healthy Subjects and Chronic Comorbid Subjects without AKI" [1]. In order to determine the specificity of [IGFBP7]·[TIMP-2] for identifying patients at risk of developing AKI we studied a cohort with nine broad classification of disease who did not have AKI. Details regarding the population that was targeted for inclusion in the study are also described. Finally, we present data on the inclusion criteria for the healthy subjects used in this investigation to determine the reference range.