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Clinical Chemistry 47: 1023-1030, 2001;
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(Clinical Chemistry. 2001;47:1023-1030.)
© 2001 American Association for Clinical Chemistry, Inc.


Articles

Cardiac Troponin T and Creatine Kinase MB Are Not Increased in Exterior Oblique Muscle of Patients with Renal Failure

Salim Fredericks1a, Joanne F. Murray2, Michael Bewick3, René Chang3, Paul O. Collinson4, Nicholas D. Carter2 and David W. Holt1

1 Analytical Unit, Cardiological Sciences, and
2 Medical Genetics Unit, St. George’s Hospital Medical School, London SW17 0RE, United Kingdom; and Departments of
3 Renal Medicine and
4 Chemical Pathology, St. George’s Hospital, London SW17 0QT, United Kingdom.

aAuthor for correspondence. Fax 44-20-8767-9687; e-mail frederic{at}sghms.ac.uk.

Background: Serum cardiac troponin T (cTnT) concentrations may be increased in patients with renal dysfunction without evidence of cardiac damage, as assessed by conventional methods. It has been suggested that these positive measurements result from the expression in skeletal muscle of fetal isoforms of cTnT, which are detected by the cTnT immunoassay.

Methods: Skeletal muscle (exterior oblique) biopsies were taken from healthy living kidney donors (n = 5) and transplant recipients (n = 19). The amounts of cTnT and creatine kinase (CK) isoenzymes in skeletal muscle of healthy controls were compared with those in patients with renal failure (Wilcoxon–Mann–Whitney test). cTnT was measured quantitatively by a second-generation assay, with a limit of detection of 1 µg/g of protein, and qualitatively by immunohistochemistry and immunoblotting. CK-MB was measured by quantitative electrophoresis.

Results: Minute quantities of cTnT were detected in 2 of the 5 (40%) control samples and 9 of the 19 (47%) renal failure samples, respectively, at mean concentrations of <5 µg/g of protein for both subject groups. This was <1/6000th that found in heart muscle. There was no significant difference in cTnT or CK-MB content in skeletal muscle between healthy controls and patients with renal failure. Increased serum cTnT did not predict detectable cTnT in skeletal muscle. cTnT was not detected qualitatively by immunoblotting or immunohistochemistry in any skeletal muscle samples.

Conclusions: Uremia does not affect the content of cTnT or CK-MB in exterior oblique muscle, suggesting that cTnT detected in serum from patients with renal failure does not originate from skeletal muscle.




The following articles in journals at HighWire Press have cited this article:


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P. O Collinson and D. C Gaze
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C. W. Hamm, E. Giannitsis, and H. A. Katus
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S. Fredericks, J. F. Murray, N. D. Carter, A. M.S. Chesser, S. Papachristou, M. M. Yaqoob, P. O. Collinson, D. Gaze, and D. W. Holt
Cardiac Troponin T and Creatine Kinase MB Content in Skeletal Muscle of the Uremic Rat
Clin. Chem., June 1, 2002; 48(6): 859 - 868.
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