Acute kidney injury without known confounders resulted in elevated troponin I and T levels above the 99th percentile in 6 of 19 subjects (31.6%).
Observational (n=19)
No
Are cardiac troponin levels elevated in subjects with acute kidney injury without known confounders?
Acute kidney injury independently influences plasma troponin levels, resulting in elevations above the 99th percentile in a subset of patients without known cardiac confounders.
AIM: To investigate and describe cardiac troponins in subjects with acute kidney injury (AKI). METHODS: A prospective observational study of troponin in subjects presenting with AKI in a tertiary hospital. Creatine kinase-MB (CKMB), troponin I (Abbott Laboratories), and troponin T (Roche 4th generation) were measured. Patients with conditions known to cause elevated troponin levels were excluded. RESULTS: Nineteen subjects were enrolled in the study. Six subjects had troponin I and T concentrations above the 99th percentile of a reference population. There was high concordance of result between troponin I and troponin T. However, the concordance of elevated troponin levels with CKMB was less marked at 45%. Statistically significant factors associated with elevated troponin levels were age over 60 years, abnormal electrocardiogram, and history of previous ischemic heart disease. CONCLUSION: This is the first study able to demonstrate impaired renal function occurring acutely, without known confounders, results in elevated troponin levels. This suggests that impaired renal function disease influences plasma troponin levels in AKI as well as in chronic kidney failure.
Song et al. (2011) conducted an observational in Acute kidney injury (n=19). Acute kidney injury was evaluated on Troponin I and T concentrations above the 99th percentile of a reference population. Acute kidney injury without known confounders resulted in elevated troponin I and T levels above the 99th percentile in 6 of 19 subjects (31.6%).