Abstract
Acute kidney injury (AKI) is a common clinical condition among hospitalized patients and has been associated with a significant increase in the risk of cardiovascular events. In this context, the interpretation of biomarkers such as high-sensitivity cardiac troponin T (hs-cTnT) presents diagnostic challenges, as its levels may rise even in the absence of acute myocardial ischemia. A recent retrospective cohort study including over 15,000 emergency department visits showed that patients with AKI were 1.8 times more likely to present elevated hs-cTnT levels without a diagnosis of acute myocardial infarction. These findings suggest that troponin elevation may result from subclinical myocardial injury or reduced renal clearance. This highlights the need for a more comprehensive diagnostic approach combining hs-cTnT with other biomarkers, such as natriuretic peptides and inflammatory markers, to improve cardiovascular risk stratification. Further research is essential to clarify the clinical significance of troponin elevation in the context of AKI, in order to optimize clinical decision-making and the prevention of adverse cardiovascular outcomes.
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