Cardiac Troponin T Is Not Detected in Western Blots of Diseased Renal Tissue

Abstract

Recent publications of consensus documents for the redefinition of myocardial infarction are heavily predicated on the role of increases in cardiac troponin (I or T) in serum in the setting of ischemic symptoms (1)(2)(3)). Cardiac troponin T (cTnT) has also been reported to be a predictor of mortality in patients with end stage renal disease (4)(5). An unexplained increase in the frequency of increased serum cTnT compared with serum cardiac troponin I has been described in these patients (6)(7). Explanations advanced for this difference include the possibility of nonspecific reactions in the cTnT assay or de novo expression of cTnT in skeletal muscle of renal diseased patients that is subsequently released into the serum (8). However, recent studies on skeletal muscle from renal disease patients have shown that although the two antibodies used in the cTnT diagnostic assay (M7 and M11.7) individually bind to muscle proteins, this would not cause false-positive results in the current-generation cTnT assay marketed by Roche (8). On the other hand, cardiac troponin I is not expressed in fetal or in healthy or diseased adult human skeletal tissue (9). An additional possibility is that cTnT or other immunoreactive proteins are being expressed in diseased renal tissue. In the current …