Troponin is a protein complex of three subunits (T, I, and C) that is involved in the contractile process of skeletal and cardiac muscle. Both cardiac and skeletal muscle express troponin C; whereas troponin T and I are generally thought to be cardiac-specific. When cardiac injury occurs (from ischemia or various other causes), cardiomyocytes release cardiac troponin into the blood in proportion to the degree of damage. Troponin levels increase within 3 to 4 hours after the onset of damage and remain high for up to 4 to 7 days (troponin I) or 10 to 14 days (troponin T). However, blood from healthy individuals with no evidence of cardiac disease also contains very low amounts of cardiac troponin. Some of the newer high-sensitivity assays may be able to measure troponin in normal individuals; although many of the commercially available assays cannot detect troponin at all or cannot quantify it at levels below the measuring range of the assay. Clinically, the most important use of troponin testing is to identify patients suspected of having an acute coronary syndrome (ACS). ACS is defined as a spectrum of conditions caused by insufficient supply of oxygen to the myocardium by the coronary arteries. However, elevated cardiac troponin levels are not specific for the diagnosis of ACS or acute spontaneous myocardial infarction (MI) (type 1 MI). Individuals with non-ACS conditions can also have elevated cardiac troponin. Non-ACS conditions can include noncoronary causes (e.g., sepsis, congestive heart failure, myocarditis, drug toxicity, pulmonary embolism, hypoxia, and global hypoperfusion) and coronary causes from ischemic imbalance i.e., increased demand in the setting of stable coronary artery disease (CAD) lesions] classified as type 2 MI. Many symptoms associated with non-ACS conditions may overlap with symptoms of ACS (e.g., chest pain or dyspnea).This presents a diagnostic dilemma to the clinician and often requires an extended evaluation before the clinician can make an accurate diagnosis. The purpose of this comparative effectiveness review will be to present information for the appropriate use of troponin levels to guide evidence-based management decisions for patients with CKD. These findings should be useful for a diverse set of contingents including cardiologists, nephrologists, emergency room physicians, and laboratory medicine scientists who use and interpret troponin testing in the clinical management of patients. Findings may also be useful for epidemiologists in tackling research gaps for further studies.