[Troponins and chronic kidney disease]

Coronary thrombosis was recognized since 19th century as clinical entity with bad outcomes; only in 1912 it was reported that acute myocardial infarction had to been distinguished from angina pectoris. First diagnostic test was electrocardiogram, while white blood cells count and erythrocytes sedimentation rate were the only available laboratory tests. Late in the 60s and 70s glutammic oxaloacetic and glutamic pyravate transaminase, lactate dehydrogenase and creatine kinase were added to biomarkers pool to provide a diagnosis of myocardial infarction related to myocardial cells injury. Only in 1987 assays for cardiac troponin were developed to assess structural damage of myocardial cells and in 2010 high sensibility troponins first dosage kits became available. It is well known that the population with chronic kidney disease (CKD) is at greater risk for cardiovascular disease and death than the general population. The use and interpretation of high sensitivity cardiac troponin (hs-cTn) assays have been particularly challenging in these patients with the majority having elevated levels at baseline. Aim of this review is to evaluate hs-cTn in patients with CKD for the diagnosis of AMI and for the prognostic significance of elevated levels in CKD patients without AMI