Abstract

Objective In patients with CKD, cTn concentrations may be elevated in the absence of AMI, which is a predicted finding caused by chronic structural heart disease rather than acute injury. The increase in troponin level observed in noncardiac conditions provides conflicting results when predicting mortality. Low lactate clearance was associated with increased mortality. Lactate clearance is calculated as follows: (early lactate − late lactate/early lactate) ∗ 100. We aimed to investigate whether troponin clearance calculated according to this formula had an effect on short-term mortality. Methods The study included 300 patients with chronic renal failure who had a sepsis-related organ failure assessment (SOFA) score ≥3. By taking the baseline troponin at the time of emergency presentation as reference and comparing them with the fourth-hour troponin values, troponin clearance was investigated in the evaluation of mortality among hospitalized patients with CKD within the first month after discharge. The data obtained were analyzed using the SPSS data analysis software version 20.0. Student's t-test was used for the parametric data, and the Chi-squared test for the nonparametric data. Results Of the 300 patients evaluated, 189 patients survived (mean age 66.20 ± 14.597 years), and 111 died (mean age 74.81 ± 12.916 years). Troponin clearance was detected in 40 of the 111 patients in the mortality group and 119 of the 189 patients in the survival group. Troponin clearance was significantly more frequent in surviving patients (P=0.0000083). Conclusion Troponin clearance can be considered as a valuable leading indicator of survival, but higher levels of troponin clearance did not lead to higher survival rates.

Highlights

  • Cardiac troponin I and cardiac troponin T, which are sensitive biological markers of myocardial injury, are used to diagnose acute myocardial infarction (AMI) [1,2,3,4]

  • In patients with chronic kidney disease (CKD), cardiac troponin (cTn) concentrations may be elevated in the absence of AMI [8], which is a predicted finding caused by chronic structural heart disease rather than acute injury [5, 6]

  • Increased cTn has been observed in the absence of acute coronary syndrome (ACS) in both cardiac and noncardiac patients. ere are additional questions concerning the causes of elevated cTn and the reasons for the observed differences between the increases in cardiac troponin T (cTnT) and Cardiac troponin I (cTnI)

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Summary

Introduction

Cardiac troponin I (cTnI) and cardiac troponin T (cTnT), which are sensitive biological markers of myocardial injury, are used to diagnose acute myocardial infarction (AMI) [1,2,3,4]. In patients with CKD, cTn concentrations may be elevated in the absence of AMI [8], which is a predicted finding caused by chronic structural heart disease rather than acute injury [5, 6]. Ere are additional questions concerning the causes of elevated cTn and the reasons for the observed differences between the increases in cTnT and cTnI. Increased cTn has been observed in the absence of acute coronary syndrome (ACS) in both cardiac and noncardiac patients. To answer these questions, it may be helpful to examine the synthesis, susceptibility, destruction, and/or clearance process of cTn [9]. It was shown that greater molecular weight (kDa) was associated with cTn

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