Serum levels of cardiac troponin I and other marker proteins in patients with chronic renal failure.
BACKGROUND
Serum levels ob biochemical markers for acute myocardial infarction (AMI) can be increased in patients with chronic renal failure (CRF) or skeletal muscle injury, creating diagnostic confusion. We evaluated the clinical utility of cardiac troponin I (cTnI) as a marker of AMI, particularly in patients with CRF.


METHODS
Subjects consisted of 59 healthy volunteers and 102 patients: 61 with CRF undergoing hemodialysis (CRF-HD), 10 with CRF under conservative therapy (CRF-CT), 21 with renal disease (RD), and 10 with muscle disease (MD). Patients with RD, CRF, and MD were evaluated to verify the absence of myocardial injury. We developed an immunoradiometric assay to measure serum cTnI using monoclonal antibodies. The lower limit of detection was 0.33 micro g/l. Serum cTnI, creatine kinase (CK), CK-MB, cardiac troponin T (first-, second-, and third-generation assay: cTnT-I, cTnT-II, and cTnT-III), and cardiac myosin light chain 1 (cMLC1) were measured.


RESULTS
cTnI was not detected in healthy volunteers or patients with CRF, RD, or MD. In patients with CRF-HD, elevated levels occurred in 4.9% (3/61) for CK, 0% (0/61) for CK-MB, 39.5% (15/38) for cTnT-I, 7.3% (3/41) for cTnT-II, 13.0% (3/23) for cTnT-III, and 77.0% (47/61) for cMLC1; and in patients with MD the levels were increased in 70% (7/10) for CK, 50% (5/10) for CK-MB, 44.4% (4/9) for cTnT-I, 20% (2/10) for cTnT-II, and 50% (5/10) for cMLC1.


CONCLUSIONS
cTnI is a highly specific marker for AMI and is particularly useful for detecting AMI in patients with CRF or MD. Serum levels of biochemical markers for acute myocardial infarction (AMI) can be increased in patients with chronic renal failure (CRF) or skeletal muscle injury, creating diagnostic confusion. We evaluated the clinical utility of cardiac troponin I (cTnI) as a marker of AMI, particularly in patients with CRF.
Nakai
Keiko
K
Department of Laboratory Medicine, Iwate Medical University, 19-1 Uchimaru, 020-8505, Morioka, Japan. keikoyn@iwate-med.ac.jp
Nakai
Kenji
K
Nagane
Yutaka
Y
Obara
Wataru
W
Sato
Michiro
M
Ohi
Kiyofumi
K
Matsumoto
Noriyuki
N
Takanashi
Naoki
N
Itoh
Chuichi
C
D015415:Biomarkers / Q000032:analysis; D016022:Case-Control Studies; D003402:Creatine Kinase / Q000097:blood; D052279:Creatine Kinase, MB Form; D006801:Humans; D007527:Isoenzymes / Q000097:blood; D007676:Kidney Failure, Chronic / Q000097:blood / Q000378:metabolism* / Q000628:therapy; D009203:Myocardial Infarction / Q000097:blood / Q000175:diagnosis; D009206:Myocardium / Q000378:metabolism*; D018994:Myosin Light Chains / Q000097:blood; D006435:Renal Dialysis; D019210:Troponin I / Q000097:blood*; D020107:Troponin T / Q000097:blood
D015415:Biomarkers; D007527:Isoenzymes; D018994:Myosin Light Chains; D019210:Troponin I; D020107:Troponin T; D003402:Creatine Kinase; D052279:Creatine Kinase, MB Form