Abstract

We challenged to identify the cutoff value of cTnT in chronic kidney disease (CKD) patients by point of care assessment way. A single center, prospective cross-sectional study was planned and performed. 201 consecutive patients who were visited emergency room for chest symptoms were enrolled in this study. All patients were performed routine practice for differential diagnosis of chest symptom by cardiologist. Simultaneously, semiquantitative measurement of cTnT was performed using same blood sampling on the blind condition to cardiologists for this study. Study patients were divided into four groups according to the estimated glomerular filtration rate (eGFR), CKD1-2, CKD3, CKD4-5, and CKD5D. Usefulness of semiquantitative measurement for diagnosing ACEs was investigated in each group. 77 (38%) of total patient was diagnosed as acute coronary events (ACEs). About 50% of patients were showing cTnT level less than 0.03 ng/mL. The cTnT level over 0.1 ng/mL was found in 30% of total subjects. Mean quantitative value of cTnT was 0.29 ± 0.57 ng/mL in total subjects. Estimated cutoff value in CKD3 patients was 0.088 ng/mL with a sensitivity of 59.3% and specificity of 80.0%. Interestingly, the cutoff values of CKD1-2, CKD4-5, and CKD5D were 0.047, 0.18, and 0.27 respectively, which are half, two times, and three times of CKD3 cutoff value 0.088. The specificities of four cutoff values in each CKD group were showing over 80%, which is higher than sensitivity, respectively. In CKD patients, semiquantitative, point of care assessment of cTnT could be a useful tool for screening for ACEs.

Highlights

  • The American Heart Association has recognized chronic kidney disease (CKD) as the strongest contributor to cardiac events

  • More chest pain/chest discomfort was found in patients with earlier stage of CKD, and converse phenomenon was observed in dyspnea

  • Median NT-proBNP level was higher in more advanced stage of CKD. 77 (38%) of total patient was diagnosed as acute coronary events (ACEs) by cardiologist

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Summary

Introduction

The American Heart Association has recognized chronic kidney disease (CKD) as the strongest contributor to cardiac events. Cardiac troponin I and T (cTnT) are components of the contractile apparatus of myocardial cells and are expressed almost exclusively in the heart. Elevations of these markers in the blood reflect injury leading to necrosis of myocardial cells.[6] it is reported that cardiac troponins are good markers for identifying myocardial necrosis, and cardiac systolic dysfunction,[7] left ventricular hypertrophy,[8] and CAD9 even in end-stage kidney disease (ESKD) patients

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