The Cardiac Troponin Renal Disease Diagnostic Conundrum: Past, Present, and Future
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Articles, see p 425 and p 436
Nearly 25 years ago, novel assays of cardiac troponin (cTn) emerged as diagnostic and prognostic blood-based biomarkers superior to creatinine kinase isoforms, utilizing the accuracy of immune-assay technology and unique cardiac myocyte-specific epitopes. A new consensus definition of acute myocardial infarction (AMI) ultimately emerged, recommending cTn as the biomarker of choice.1 This definition reflected an increased emphasis on a biochemical basis for the diagnosis of AMI, particularly for non-ST–elevation AMI (NSTEMI). Two subsequent redefinitions of AMI have further emphasized and refined the role of cTn levels for diagnosis. Most recently, the European Society of Cardiology guidelines, utilizing an extended experience with high-sensitive (hs) cTn assays, have proposed algorithms to triage patients suspected of NSTEMI based on initial, or initial and 1-hour follow-up hs-cTn levels.2 Both groups presenting their work in this issue of Circulation have previously contributed3,4 to demonstrating the efficacy of such an approach. However, as all clinicians know, the interpretation of cTn levels for the diagnosis of NSTEMI often requires considerable clinical acumen to account for confounding comorbidities. These challenges have led to some trepidation surrounding the introduction of hs-cTn assays into clinical practice in the United States. No comorbidity has resulted in more confusion regarding cTn result interpretation than chronic kidney disease (CKD).5
Soon after the first studies demonstrating a poor prognosis in unstable angina patients with elevated cardiac troponin T (cTnT) quantified by first-generation assays, investigators observed that cTnT levels could be chronically elevated in patients with CKD without signs or symptoms of AMI.6 These findings were initially attributed to a lack of cardiac isoform specificity; however, subsequent versions of the cTn assays …