**7. Other cardiac biomarkers: Troponin T**

Cardiac troponins are regulatory proteins within the myocardium that are released into the circulation when damage to the cardiomyocite has occurred. Therefore, serum troponin is an exquisitely sensitive marker of myocardial injury during the acute coronary syndrome and is necessary for establishing the diagnosis of myocardial infarction (Daubert et al., 2010).

Cardiac troponins control the calcium-mediated interaction of actin and myosin, which results in contraction and relaxation of striated muscle. The troponin complex is made up to three subunits: troponin C, troponin I and troponin T. Troponin C is expressed by cells in both cardiac and skeletal muscle. In contrast, troponin I and T are unique to cardiac muscle.

Among patients with acute coronary syndrome, cardiac troponin has not only diagnostic value, but yield prognostic information as well. It has been proven to be a potent independent indicator of recurrent ischemic events and an estimate for the risk of death among patients presenting with acute coronary syndrome (Heidenreich et al., 2001).

Persistently elevated cardiac troponin is frequently observed among asymptomatic patients with end-stage-renal-disease and is associated with increased mortality (Apple et al., 2002; de Fillipi et al., 2003; Ogi et al., 2001). There has been proposed several mechanisms for explaining the high levels of troponin among patients with CKD. Although troponin is a relative large molecule which is believed to be cleared by the reticuloendothelial system, more recent evidence suggest that troponin T is fragmented into molecules small enough to be renally excreted, which may partly explain the high prevalence of troponin T elevation in patients with renal failure (Diris et al., 2004).

Fig. 3. Evolution over time of CRP values among patients distributed in high quartile at baseline (CRP high) and those distributed in other basal quartiles (CRP). \* p<0.05 vs baseline

Cardiac troponins are regulatory proteins within the myocardium that are released into the circulation when damage to the cardiomyocite has occurred. Therefore, serum troponin is an exquisitely sensitive marker of myocardial injury during the acute coronary syndrome and is necessary for establishing the diagnosis of myocardial infarction (Daubert et al.,

Cardiac troponins control the calcium-mediated interaction of actin and myosin, which results in contraction and relaxation of striated muscle. The troponin complex is made up to three subunits: troponin C, troponin I and troponin T. Troponin C is expressed by cells in both cardiac and skeletal muscle. In contrast, troponin I and T are unique to cardiac muscle. Among patients with acute coronary syndrome, cardiac troponin has not only diagnostic value, but yield prognostic information as well. It has been proven to be a potent independent indicator of recurrent ischemic events and an estimate for the risk of death

Persistently elevated cardiac troponin is frequently observed among asymptomatic patients with end-stage-renal-disease and is associated with increased mortality (Apple et al., 2002; de Fillipi et al., 2003; Ogi et al., 2001). There has been proposed several mechanisms for explaining the high levels of troponin among patients with CKD. Although troponin is a relative large molecule which is believed to be cleared by the reticuloendothelial system, more recent evidence suggest that troponin T is fragmented into molecules small enough to be renally excreted, which may partly explain the high prevalence of troponin T elevation in

among patients presenting with acute coronary syndrome (Heidenreich et al., 2001).

levels. Data expressed as mean ± standard error.

**7. Other cardiac biomarkers: Troponin T** 

patients with renal failure (Diris et al., 2004).

2010).

Cardiac microinfarctions and arrhythmia have also been suggested as possible causes of elevations of troponin among patients with CKD.

More recently, it has been observed that CKD patients with high troponin T concentrations had clear evidence of myocardial dysfunction and raised left ventricular filling pressure (Sharma et al., 2006), supporting that volume and pressure overload can cause excessive ventricular wall tension with resultant myofibrillary damage or cardiomyocites death (Horwich TB et al., 2003). In this way, a strong association between troponin T and NTproBNP has been observed in hemodialysis patients (figure 4) (Ortega et al., 2009) and both troponin T and NT-proBNP levels has been observed to be higher in volume-overloaded CKD patients (Sommerer et al., 2007).

Fig. 4. Regression graph demonstrating the correlation between NT-proBNP and troponin T values at baseline (r: 0.4; p= 0.002)

Thus, it seems that the increased troponin T in a high proportion of patients with CKD could be related to myocardial injury induced by an increased left ventricular volume especially in those patients with diastolic dysfunction, in whom a small increase in end-diastolic volume produces an exaggerated increment in end-diastolic pressure with the subsequent myocardial damage. Furthermore, in hemodialysis patients, a strategy of strict volume control over time could significantly reduce the troponin T levels especially in those patients with higher biomarker levels at baseline, probably those with more severe myocardial dysfunction (figure 5) (Ortega et al., 2009).

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Fig. 5. Evolution over time of troponin T values among patients distributed in the high quartile at baseline (Troponin T high) vs those distributed in the other basal quartiles (Troponin T). \* p<0.05 vs baseline levels. Data expressed as mean ± standard error.
