Atherosclerotic cardiovascular disease (ASCVD) occurs commonly among end-stage renal disease (ESRD) patients due in part to the high prevalence of hypertension, carbohydrate intolerance, and lipid abnormalities in this patient population (1-4). Cardiovascular events including acute myocardial infarction (MI) and sudden cardiac death account for 21.9 to 39.0% of deaths in ESRD patients in the United States and Europe (5-9).Although MI may be diagnosed readily in patients presenting with an appropriate history of protracted chest pain and characteristic ECG findings, this diagnosis may be quite difficult in patients with atypical chest pain or preexisting ECG abnormalities such as left ventricular hypertrophy or left bundle branch block. While the ECG is highly specific (100%) in the diagnosis of MI, numerous investigators have documented its lack of sensitivity (63-82%) (10-17). During the past decade, the efficiency of diagnosing MI has been improved by the routine availability of serum creatine kinase (CK) and lactate dehydrogenase (LDH) isoenzymes.This review will address our current knowledge of the CK isoenzyme system including techniques used for isoenzyme quantitation and its role in the diagnosis of MI. Additionally, we will discuss those abnormalities in CK isoenzymes reported in ESRD patients, their pathogenesis, and how they may influence our ability to diagnose acute MI in our dialysis patients.
Historical PerspectiveCreatine kinase is a dimeric intracellular enzyme (MW 86,000 daltons) which catalyzes the reversible phosphorylation of creatine by ATP. Varying combinations of the M and B monomers produce the three major CK isoenzymes-CK-MM, CK-MB, and CK-BB. CK-MM is the predominant isoenzyme in both cardiac and skeletal muscle ( 17-20). CK-MB accounts for 15 to 40% of total CK activity in cardiac