Abstract

The last 10 years have witnessed radical changes in the definition and diagnosis of the acute coronary syndrome (ACS), including myocardial infarction, as a result of the introduction of sensitive and specific markers of myocardial damage, the cardiac troponins. One barrier to the universal acceptance of these markers has been the observation that troponin T (cTnT) concentration is commonly increased in the presence of renal failure. Initially it was believed that this constituted an important false positive limitation of the test. This was confounded by problems with the initial cTnT assay and by the observation that troponin I (cTnI) was generally not increased in these patients. However, it has recently been demonstrated that the prognostic significance of a raised cTnT concentration in patients with a suspected ACS is unaffected by renal impairment. Further, powerful outcome studies are now being reported demonstrating that raised concentrations of serum cTnT are predictive of mortality in haemodialysis patients. This review summarizes our current understanding of the prevalence and significance of raised serum cTnT concentrations in patients with kidney disease and highlights areas where our understanding is incomplete. Evidence suggests that raised troponin concentrations in uraemic patients do indeed reflect myocardial injury. In the future, patients demonstrating this abnormality may be the target for more aggressive cardiac intervention, the advantages of which have been demonstrated in the non-uraemic population.

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