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Clinical Chemistry 44: 930-938, 1998;
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Right arrow Proteomics and Protein Markers
(Clinical Chemistry. 1998;44:930-938.)
© 1998 American Association for Clinical Chemistry, Inc.

Enzymes and Protein Markers

Cardiac troponin T in patients with end-stage renal disease: absence of expression in truncal skeletal muscle

Christlieb Haller1, Jörg Zehelein1, Andrew Remppis2, Margit Müller-Bardorff2, and Hugo A. Katus2,a

1 Department of Medicine III, University of Heidelberg, 69115 Heidelberg, Germany.

2 Department of Medicine II, University of Lübeck, 23538 Lübeck, Germany.
a Address correspondence to this author at: Department of Internal Medicine II, University of Lübeck, Ratzeburger Allee 160, D-23538 Lübeck Germany. Fax 49-451-5006437.

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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