To the Editor:

We are grateful for the comments and interest of Dr Cakar M. and his collaborators regarding our study entitled “Cardiac troponin I and creatine kinase MB isoenzyme in patients with chronic renal failure” in which we included 484 consecutive chronic renal failure (CRF) patients with suspected acute coronary syndrome (ACS). Due to CRF patients being a high cardiovascular risk population, we decided to apply a strategy to improve diagnostic sensitivity and we obtained a cardiac troponin I (cTnI) cut-off value that was significantly different from that used for the general population to diagnose ACS, although it had been reported that by decreasing the 99th percentile of cTnI (cut-off value), more patients with ACS1 at risk of recurrent myocardial infarction (MI) or death would be identified, but the diagnosis of MI would increase by 47%.2

Moreover, it is important to know that any cardiac damage may cause the release of troponins from myocytes as complexes or as free troponin in circulation and there are many causes of increased troponins that are not related to ACS, among which are: 1) cardiac causes (congestive heart failure, tachycardia, left ventricular hypertrophy, myocardial contusion, myocarditis, pericarditis, cardiac amyloidosis, heart surgery, cardioversion, percutaneous coronary intervention, coronary vasospasm, radiofrequency ablation, other), 2) non-cardiac causes (chronic renal failure, sepsis, stroke, pulmonary embolism, primary pulmonary hypertension, critically ill patients, chemotherapy, sympathomimetic agents, intense resistance exercise, other) and 3) methodological causes (fibrin, haemolysis, heterophile antibodies, rheumatoid factor, other).3,4

In patients with CRF, the mechanisms that may explain the nonspecific increases in cTnI are mainly further heart damage and decreased kidney function.5 In our study, the main causes of increased cTnI in the Other Cardiac Pathologies (OCP) group were congestive heart failure, atrial fibrillation and tachycardia, while in the Other Non-cardiac Pathologies (ONCP) group they were high blood pressure, stroke and pneumonia, but we believe that all the causes described should be taken into consideration as potential confounding factors whenever high cTnI concentrations are found in patients with CRF and an absence of ACS.

Conflicts of interest

The authors declare that they have no conflicts of interest related to the contents of this article.