Troponin I and T are reliable and preferred markers for cardiac damage in patient population with NORMAL renal function.
Troponin T (TnT) is typically elevated in chronic renal failure. There are several theories with no strictive measurements on how this is diagnosed. From what I have read, most cardiologists seem to think it is due to myocardial stunning, which produce higher levels of an unbound cytosolic pool of TnT (myocardial stunning is defined as a 20% reduction in segmental wall motion at rest with evidence of recovery after hemodialysis).
Other theories include left ventricular hypertrophy, endothelial dysfunction, loss of membrane integrity due to the leakage of troponin, ongoing microinfarctions, and sub-slinical cardiac damage exacerbated by reduced renal clearance. Overall, the concentration of TnT is directly related to the GFR/renal clearance.
Regardless of the cause, studies have shown an increase in mortality in renal failure patients whose troponins are elevated; elevations in TnT are predictors of increased mortality and worsening long term cardiovascular outcomes, especially in the presence of known coronary artery disease. The question remains when to treat elevated troponins in the absence of cardiac-related symptoms; some question the need for more aggressive therapy for atherosclerotic disease or PCI in the asymptomatic patient. Post-ischemic cardiac dysfunction can occur following hemodialysis, so it is recommended to obtain baseline markers prior to this.
The best advice is to monitor serial troponins and EKG changes; many of ESRD patients have cardiomyopathy in the setting of left ventricular hypertrophy.