Cardiac troponin-I accurately predicts myocardial injury in renal failure.
BACKGROUND
Non-specific elevations of creatine kinase isoenzymes (CK-MB) and cardiac troponin-T may be seen in renal failure, confusing the diagnosis of myocardial infarction. Cardiac troponin-I (cTn-I) has been shown to be specific for myocardial damage in several disease states, but has not been prospectively evaluated in the setting of renal failure.


METHODS
This prospective case series evaluated 56 patients with acute or chronic renal failure or end-stage renal disease to assess the sensitivity and specificity of cTn-I for detecting myocardial injury in this patient population. During a 6-month period, patients admitted with suspected myocardial injury by history, physical examination, and electrocardiography were evaluated. Cardiac troponin-I (cTn-I) measurements were assessed between 8 and 48 h after admission. Appropriate medical care and further cardiac testing (echocardiography, stress testing, or arteriography) was performed at the discretion of the primary physician.


RESULTS
Myocardial injury was diagnosed in 18/56 (32%) patients by positive cTn-I levels, while only 7/56 (13%) patients had evidence of myocardial damage by CK-MB. Twenty-one of 56 (38%) patients had indeterminate CK-MB levels and 53% of these patients demonstrated myocardial ischaemia on follow-up testing. Sixteen patients had negative cardiac studies; all of these patients had negative cTn-I levels, while seven of these 16 (44%) patients had indeterminate CK-MB measurements. All of the patients with positive cTn-I levels had positive cardiac studies. Positive troponin levels were associated with increased in-hospital mortality. Sensitivity and specificity for CK-MB were 44 and 56% respectively, and 94 and 100% for cTn-I.


CONCLUSIONS
These data support the use of cTn-I for diagnosing myocardial injury in patients with renal failure. Elevated cTn-I levels are associated with increased short-term mortality in renal failure patients. The accuracy of cTn-I could potentially limit unnecessary cardiac testing in renal failure patients, while the enhanced sensitivity contributes to risk stratification and aids in diagnosing true myocardial injury in this population susceptible to non-specific elevations in other muscle enzymes.
Martin
G S
GS
Department of Internal Medicine, Vanderbilt University Medical Center, Nashville, Tennessee 37232-2650, USA.
Becker
B N
BN
Schulman
G
G
D058186:Acute Kidney Injury / Q000097:blood* / Q000150:complications; D003402:Creatine Kinase / Q000097:blood; D003951:Diagnostic Errors; D005260:Female; D006335:Heart Injuries / Q000097:blood / Q000150:complications / Q000175:diagnosis; D006801:Humans; D007527:Isoenzymes; D007676:Kidney Failure, Chronic / Q000097:blood* / Q000150:complications; D008297:Male; D008875:Middle Aged; D009203:Myocardial Infarction / Q000097:blood* / Q000150:complications / Q000175:diagnosis*; D009206:Myocardium / Q000201:enzymology / Q000378:metabolism*; D011446:Prospective Studies; D012680:Sensitivity and Specificity; D019210:Troponin I / Q000097:blood*
D007527:Isoenzymes; D019210:Troponin I; D003402:Creatine Kinase