956High-sensitivity troponin I predicts the risk of adverse outcomes in patients with chronic kidney disease

Abstract

Background: Cardiovascular disease (CVD) is the most common cause of death in patients with chronic kidney disease (CKD). Because troponin accumulates in CKD, its use in patients with acute myocardial infarction (AMI) remains problematic. Recently developed assays for high-sensitivity troponin I (hs-TnI) have shown that its elevated levels predict adverse outcomes in the general population and those with stable CVD. Whether hs-TnI levels can be utilized to predict adverse events in those with CKD remains unknown. Purpose: We examined the prognostic value of hs-TnI in patients with and without CKD. Methods: We measured hs-TnI levels and renal function in 4,017 patients, free of AMI undergoing coronary angiography. Cox proportional hazard models adjusted for clinical variables (age, sex, race, smoking, body mass index, diabetes, hypertension, hyperlipidemia, prior myocardial infarction, heart failure, coronary disease severity, aspirin, beta blockers, angiotensin converting enzyme inhibitors/angiotensin receptor blockers, statins and high sensitivity C-reactive protein levels) were used to analyze the association between hs-TnI and risk of cardiovascular death and all cause death. Results: Of 4,017 patients (mean age, 64 years; 63% men; 20% blacks) enrolled, 999 (25%) had CKD (estimated glomerular filtration rate (eGFR) <60 mL/min/1.73 m2 or urine albumin/creatinine ratio >30 mg/g). Over a median follow-up of 4.8 years, there were 440 (11%) cardiovascular and 735 (18%) all-cause deaths. In a multivariate model adjusted for all clinical variables, cardiovascular and all-cause mortality were significantly higher in those with higher hs-TnI levels (P<0.001). For each doubling of hs-TnI level, the risk of CV death [HR 1.18 (1.11, 1.25) in those without CKD and 1.25 (1.17, 1.34) in those with CKD] and all cause death [HR 1.13 (1.08, 1.19) in those without CKD and 1.23 (1.17, 1.30) in those with CKD, all p<0.001] were higher. Hs-TnI was a stronger predictor of all-cause mortality in patients with CKD compared to those without CKD (p-interaction 0.023). Conclusion: HsTnI is an important marker of adverse cardiovascular outcomes in patients with and without CKD and is a stronger predictor in those with CKD. Thus, hs-TnI levels identify CKD patients at greater risk in whom aggressive management may be warranted.