Coronary artery disease is highly prevalent in patients with endstage renal
disease, and accounts for much of their observed morbidity and mortality.
Despite this, diagnosing myocardial disease in this population remains prob
lematic, because many patients present with abnormal baseline electrocardio
grams, frequently compounded by silent or atypical symptoms. Conventionally
used enzymatic markers of cardiac injury have not resolved this dilemma be
cause of their poor specificity in end-stage renal disease. In particular,
nonspecific elevations in creatinine kinase-muscle brain enzyme, a widely a
ccepted marker of cardiac injury, have been consistently observed in the ab
sence of other demonstrable evidence for cardiac injury. Recently, the card
iac troponins (troponin I and troponin T) have emerged as more senstitive m
arkers for cardiac ischemia, facilitating rapid bedside diagnosis and early
risk stratification. Unfortunately, cardiac troponin T shows poor specific
ity in endstage renal disease, possibly because of variable expression in e
xtracardiac tissues. On the other hand, troponin I consistently maintains a
high sensitivity and specificity, and is the most sensitive marker for isc
hemic heart disease in this patient population, Curr Opin Nephrol Hypertens
8:719-722. (C) 1999 Lippincott Williams & Wilkins.