Cardiac troponin T in patients with end-stage renal disease: absence of expression in truncal skeletal muscle
Author(s) -
Christlieb Haller,
Jörg Zehelein,
Andrew Remppis,
Margit Müller-Bardorff,
Hugo A. Katus
Publication year - 1998
Publication title -
clinical chemistry
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.705
H-Index - 218
eISSN - 1530-8561
pISSN - 0009-9147
DOI - 10.1093/clinchem/44.5.930
Subject(s) - troponin complex , medicine , end stage renal disease , cardiology , troponin t , coronary artery disease , cardiac muscle , kidney disease , troponin , skeletal muscle , disease , myocardial infarction
In patients with end-stage renal disease (ESRD), the serum concentration of cardiac troponin T (cTnT) may be increased without cardiac ischemia. One reason for this unexplained increase could be the extracardiac expression of cTnT. However, truncal skeletal muscle biopsies of five patients with ESRD showed no evidence of the expression of either cTnT mRNA (reverse transcription-PCR) or protein (immunoblot, immunofluorescence). We also measured the serum concentration of cTnT in 97 patients with ESRD. The serum cTnT concentration determined in both first and second generation cTnT assays was significantly lower P <0.01 in patients with a low cardiac risk than in patients with positive indicators of coronary artery disease. The correlation between cTnT and indicators of coronary artery disease is consistent with the hypothesis that cTnT in the serum of patients with ESRD originates from the heart.
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