Abstract
Assessing emergency department (ED) patients with reduced kidney function for possible myocardial infarction (MI) is challenging. Troponin is a marker of myocardial injury rather than MI itself, and patients with chronic kidney disease (CKD), acute kidney injury (AKI), or age-related reductions in glomerular filtration rate (GFR) often have higher baseline troponin concentrations. When a troponin concentration is above a conventional decision threshold (e.g., the laboratory upper reference limit [URL]), accelerated diagnostic pathways are more likely to direct patients toward serial testing, cardiology consultation, admission, or further cardiac investigation. Conversely, there is a risk that clinicians may incorrectly dismiss a raised troponin concentration as simply being due to kidney dysfunction and thereby under-recognize acute MI.