The measurement of the cardiac troponins has produced a paradigm shift in the management of cardiac disease. Elevation of cTn without acute myocardial infarction (AMI) also occurs in non-cardiac patients including those with chronic kidney disease (CKD). Cardiovascular disease accounts for 50% of mortality in CKD. In this thesis, the prognostic value of cTn elevation in CKD was investigated by meta-analysis of published data and recruitment of a CKD cohort. The relationship between elevated cTn and cardiac imaging; the involvement of inflammation, oxidative stress and platelet activation were investigated. The difference in cTn pre and post haemodialysis was investigated. The forms of cTn released into the circulation in CKD was investigated and compared to the forms released following AMI. CKD patients positive for cTn are three times more likely to die than cTn negative patients. Elevated cTn was not associated with extent of cardiac pathology but rather the presence of diffuse global ischemia. Elevated cTn in CKD is associated with increased C-reactive protein but not other markers of inflammation, oxidative stress or platelet activation. cTn, CRP and interleukin-6 were predictive of all-cause mortality. Following dialysis, cTnl but not cTnT adsorbs to the membrane within the vascular compartment. Intact cTnT and cTnl were observed in CKD patient serum by Western blotting, which is similar to the cTn forms of observed following myocardial infarction. Some lower molecular weight fragments are demonstrable but their presence is method dependent and heterogeneous between patients. Elevated cTn is of prognostic value in CKD and reflects the high incidence of cardiovascular disease and cardiac death. Elevated cTn is not a false positive. The mechanism of cTn release in CKD remains to be understood. The clinical challenge is for the renal physician to translate the potential for cardiovascular disease monitoring conferred by cTn into improved patient management.