DOI: 10.36347/sjams.2020.v08i01.040

Pages: 212-215

The Kidney Disease Outcomes Quality Initiative (KDOQI) of the National Kidney Foundation (NKF) established a definition and classification of CKD in 2002. Kidney disease is the ninth leading cause of death in the United States. Coronary artery disease (CAD) is the major cause of death in patients with chronic kidney disease (CKD), responsible for up to 45% of overall mortality. The biochemical diagnosis of myocardial infarction in patients with CKD is always complicated by the fact that serum markers of myocardial necrosis such as creatine kinase, MB-fraction of creatine kinase. (CK-MB) are commonly increased in end stage CKD patients, even in the absence of clinically suspected myocardial infarction. Cardiac troponin (cTn) is a component of the contractile apparatus of the cardiac muscle. Because of its high tissue specificity, cTn is a cardio-specific, highly sensitive marker of myocardial damage. However, increases in serum cTn concentration have been reported in patients with CKD in the absence of acute myocardial infarction. Various study suggest that Elevations of cTnI not associated with ACS were common in patients with CKD stage 3 to 5, and there was an increase in mortality with higher concentrations of cTnI. Objective: To assess the elevated level of cardiac troponin in patients of Chronic kidney Disease stage 3 to above, on and off Haemodialysis