24 The persistent myocardial necrosis that leads to an elevated troponin in patients on dialysis has been attributed to left ventricular hypertrophy61 or coronary artery atherosclerosis.2 However, studies www.selleckchem.com/products/Romidepsin-FK228.html using cardiac magnetic resonance imaging have demonstrated that troponin may be high without evidence of myocardial infarction, suggesting that pathologies such as microcirculatory disturbances or increased sympathetic tone may explain the increase in troponin.62 Although there is strong evidence that elevated troponin confers a poorer prognosis in an asymptomatic patient undergoing dialysis,

there is currently no evidence to support biomarker-guided therapy for the individual patient. The most practical reason for measuring troponin in this context is to determine a ‘baseline’ level for each patient that can be referred to if the patient subsequently presents with cardiac symptoms. Whether cTnT or cTnI is measured in this context is not as important as that the same assay be used subsequently. As a tool for identifying patients

at risk, cTnT may be superior to cTnI because the evidence is more robust and interpretable for this assay, largely because of better standardization of assays than cTnI, and selleck screening library because measuring cTnT with current assays will identify more patients at risk. However, elevated cTnI had a stronger mortality association than cTnT in one large study, although this may be due to the chosen cut-off for cTnI being higher than that used for cTnT because of different assay characteristics.43 The performance of troponin assays continues to improve and ‘high-sensitivity’ assays are being developed

that may make the proportion of patients receiving dialysis with elevated cTnI more similar to that with elevated cTnT.22 Regardless of the differences between assays or why the troponin was measured, an abnormal troponin level should underscore the need to carefully review the patient, who is at least twice as likely to die as the patient without elevated troponin. Elevated levels of BNP are also Vildagliptin associated with poorer survival in patients undergoing both haemodialysis43,47,48 and peritoneal dialysis.44,63 The association of NT-BNP-76 with mortality was independent of left ventricular ejection fraction in one study44 and both NT-BNP-76 and extracellular fluid volume overload were independent predictors of cardiovascular mortality in another.64 Patients whose NT-BNP-76 increased at 90 days in the highest tertile of change (≥429 ng/L) had a more than twofold risk of death compared with patients experiencing the lowest tertile of change.47 Although most studies measured NT-BNP-76, higher levels of BNP-32 are also associated with mortality.5 Potential causes of elevated BNP levels in patients undergoing dialysis include systolic dysfunction,5 diastolic dysfunction,65 increased left ventricular mass49 and coronary artery disease.