Cardiac Troponins in Chronic Kidney Disease: A Marker of Global Cardiovascular Risk

above the detection limit signifying cardiac myonecrosis may be related to sources other than acute MI and may be unexplained by decreased biomarker clearance alone. Although the pathogenesis of troponin release from myocytes has yet to be fully elucidated, potential contributing mechanisms include pre-existing CV disease (e.g., stable epicardial coronary artery disease, heart failure, left ventricular hypertrophy), subendocardial ischemia, direct myocardial toxicity from uremia (and its associated toxins), and hemodialysis-related stressors [2] . These intervening processes limit the specificity and diagnostic utility of static measurements of troponin in patients with CKD with acute MI. Clear guidance regarding the optimal management approach to elevated troponins in CKD is lacking. In 2012, the universal definition of MI put forth by the Third Global MI Task Force represented a concerted effort to provide a structured classification scheme and standardize the use and application of cardiac troponins in a broad range of clinical scenarios [3] . Importantly, the multidisciplinary consensus committee emphasized the need for adjunctive evidence of myocardial ischemia and assessment of the trajectory of this biomarker to further hone the diagnosis of MI. In this issue of the American Journal of Nephrology , Vasudevan et al. [4] carefully apply this suggested approach to a sample of 430 patients presenting with suspected MI who were enrolled in the prospective, multi-center Performance of Triage Cardiac Markers in the Clinical Setting (PEARL) study. This Approximately 15% of people in the US live with chronic kidney disease (CKD) and ∼ 500,000 patients require chronic hemodialysis [1] . Despite encouraging recent trends of steady declines in overall mortality in Medicare patients with CKD, cardiovascular (CV) disease continues to account for more than half of the deaths in patients with end-stage renal disease (ESRD) [1] , and as such, optimization of CV outcomes in this population remains a major treatment goal. Cardiac troponin measurement plays important roles in the early identification, risk stratification, prognostication, management, and monitoring of acute myocardial infarction (MI) in the overall population. However, their frequent elevation in patients with CKD, coupled with the recent advent of newer-generation and increasingly sensitive troponin assays, has made timely and accurate diagnosis of MI in this population challenging. Since elevated troponins are commonly encountered in patients with CKD, we highlight important considerations regarding their practical application in contemporary practice in this high-risk population.