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(Circulation. 2005;112:3036-3037.)
© 2005 American Heart Association, Inc.

Editorial

Cardiac Troponins and Renal Failure

The Evolution of a Clinical Test

Michael S. Lauer, MD

From the Departments of Cardiovascular Medicine, Cleveland Clinic Foundation and Epidemiology and Biostatistics, Case Western Reserve University, Cleveland, Ohio.

Reprint requests to Michael S. Lauer, MD, FACC, FAHA, Desk JJ40, 9500 Euclid Ave, Cleveland Clinic Foundation, Cleveland, OH 44195. E-mail Lauerm@ccf.org

Key Words: Editorials • kidney • prognosis • mortality

An extract of the first 250 words of the full text is provided, because this article has no abstract.

In this issue of Circulation, Khan and colleagues present the results of an elegantly performed meta-analysis of the prognostic implications of elevated levels of troponin T and I among asymptomatic patients with end-stage renal disease.¹ After systematically collating the results of 28 cohort studies involving 3931 patients, they noted that an elevated troponin T level identified a group of end-stage renal disease patients with high mortality risk. Although elevated troponin I was also associated with increased risk, the exact effect size was difficult to assess because of a lack of standardization of current assays. The authors noted that despite the consistent association between elevated troponin T and mortality, the effect might be overestimated because of publication bias and study heterogeneity. Nonetheless, this meta-analysis, along with the specific reports of the largest published cohort studies,^2,3 provides robust evidence that troponin T elevation in the setting of end-stage renal disease is ominous.

Article p 3088

The development of troponin measurement in the absence of end-stage renal disease is an excellent paradigm for the modern evolution of clinical tests. Troponin T and troponin I are both integral parts of the cardiac muscle infrastructure and play critical roles in excitation-contraction coupling.⁴ The diagnostic importance of troponin elevation stems from its release into the bloodstream when there is some type of damage to cardiac myocyte cell-wall integrity.⁵ The high sensitivity of troponin for detecting even small myocardial infarctions has led to widespread recommendations for its routine measurement for the diagnosis of myocardial infarction.⁶ It . . . [Full Text of this Article]

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