Cardiovascular complications represent the predominant cause of death in patients in the terminal stage of renal failure. Increased concentrations of cardiac troponin T (cTnT) may be a valuable predictor of cardiac risk (1)(2). However, cardiac troponin I (cTnI), clinical symptoms, and electrocardiogram (ECG) indications may be absent in patients with a positive cTnT. This may be attributable to instability of the cTnI molecule (3) or dissimilar glomerular filtration of cTnT and cTnI (4). Positive cTnT values are of cardiac origin because the second generation of cTnT assays will not detect cTnT isoforms expressed in the skeletal muscle of hemodialysis patients (5). We therefore measured the cardiac troponins cTnT and cTnI in the plasma and urine of selected patients differing in their kidney function. We examined 24 patients with increased plasma cTnT. Patients were grouped according to their basic disease and renal function as follows: Group A included five patients (patients 1–5) who had suffered an acute myocardial infarction and three patients (patients 6–8) with cardiac damage as a result of heart surgery, all with normal or only slightly restricted glomerular filtration rate of >80 mL/min. All eight patients were male, with a mean (SD) age of 63 (11) years. Patients had clinically typical chest pain (with the exception of patient 8), and electrocardiography (ECG) showed signs of old myocardial infarction, signs of ST-segment reduction or elevation >0.1 mV with and without chest pain, or signs any arrhythmia of unknown origin. Group B included two patients (patients 9 and 10) who had suffered an acute myocardial infarction and six patients (patients 11–16) with cardiac damage as a result of heart surgery; all had a substantially restricted glomerular filtration rate (only patient 9 had values for creatinine and creatinine clearance that were within the appropriate reference intervals). All patients in …