Abstract
BACKGROUND: The onset of chronic kidney disease (CKD) results in a high level of cardiovascular morbidity and mortality. Conventional risk assessment systems tend to fail in considering the cardiovascular risk of this group of people. A biomarker of myocardial damage, high-sensitivity cardiac troponin I (hs-cTnI), has become a candidate biomarker of subclinical cardiac damage. MATERIALS AND METHODS: A prospective observational study was carried out of 120 patients with CKD stages 3 to 5 that excluded dialysis patients. A high-sensitivity immunoassay was used to measure the baseline value of hs-cTnI. The follow-up was thorough, with patients being kept under observation after 12 months of occurrence in their patients major adverse cardiovascular events (MACE), i.e., myocardial infarction, heart failure hospitalization, and cardiovascular death. RESULTS: Out of 120 CKD patients (mean age 58.2+/- 9.6 years; 62 males), 48 patients (40%) had elevated hs-cTnI (>19.0 ng/L). The number of patients who developed MACE at the time of the follow-up was 29 (24.2%). There was a significantly greater proportion of MACE in an elevated hs-cTnI group (52.1%) than in a normal hs-cTnI group (10.4%) (P < 0.001). The Cox regression analysis indicated that an independent outcome predictor of MACE was hs-cTnI (HR 3.89, 95% CI 1.91793, P = 0.002). The ROC area under the curve of hs-cTnI at predicting MACE was 0.81 (95% CI 0.7290). CONCLUSION: High-sensitivity T-I is a good prognostic biomarker of cardiovascular events among CKD patients. Its regular evaluation can help in the initial classification of risks and selective cardiovascular preventive interventions.