Creatine Kinase Subf orm Analysis in Hemodialysis Patients without Acute Coronary Syndromes

Robbins, Michael J.; Epstein, Edward; Shah, Sanjay

doi:10.1159/000190194

Cited by 24 publications

(15 citation statements)

References 6 publications

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“…False positive increases of both myoglobin and CK-MB have previously been reported in the literature. [27][28][29] Troponins are recognized to be more sensitive markers compared to myoglobin and CK-MB in that sense, but still the data on value of different subgroups of troponins display conflicting results. Several studies suggest that cTnT is more frequently elevated than cTnI in dialysis patients in the absence of myocardial damage and cTnI seems to be a more specific marker than CK-MB or cTnT in diagnosis of acute MI.…”

Section: Discussionmentioning

confidence: 99%

Predictive markers of asymptomatic atherosclerosis in end-stage renal disease patients

Mutluay¹,

Konca²,

Erten³

et al. 2010

Renal Failure

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Objective: Uremia is associated with accelerated atherosclerosis and increased cardiovascular mortality in patients with end-stage renal disease (ESRD). Cardiac injury markers, such as myoglobin, creatine kinase-MB (CK-MB), or troponins, frequently used to recognize acute coronary events, may be falsely elevated in this patient group. In this study, our aim was to (i) test serum levels of myoglobin, CK-MB, and troponin I (cTnI) in ESRD patients without coronary artery disease (CAD) and compare the results with healthy controls and (ii) to investigate the association between these markers and carotid artery intima-media thickness (CA-IMT), high-sensitive C-reactive protein (hs-CRP), and serum uric acid (SUA) levels in ESRD patients. Materials and methods: Fifty-two ESRD patients (25 hemodialysis and 27 peritoneal dialysis) and 17 healthy controls were included in the study. Serum levels of myoglobin, CK-MB, and cTnI were measured and ultrasonographic CA-IMT was determined in all participants. SUA and hs-CRP levels were only measured in the ESRD group. Results: Serum myoglobin, CK-MB levels, and the mean CA-IMT were significantly higher in ESRD group (p < 0.01), whereas cTnI levels were not different compared to healthy controls (p = 0.70). There was also a positive correlation between CA-IMT and cTnI levels (p = 0.003, r = 0.35) and CA-IMT and hs-CRP (p = 0.03, r = 0.30) or SUA levels (p = 0.003, r = 0.43). Conclusion: cTnI may serve as a more sensitive marker in detecting cardiovascular events in patients with renal failure. Besides the traditional risk factors of atherosclerosis, cTnI, hs-CRP, and SUA may have a predictive role in recognizing premature atherosclerosis in ESRD patients.

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Section: Discussionmentioning

confidence: 99%

Predictive markers of asymptomatic atherosclerosis in end-stage renal disease patients

Mutluay¹,

Konca²,

Erten³

et al. 2010

Renal Failure

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“…A baseline troponin level is essential for the proper interpretation of post-PCI elevations. 109,110 • Troponin measurement every 6-8 hours for 24 hours is ideal. 111 • Only one troponin assay should be used given the heterogeneity of assays.…”

Section: Troponin After Percutaneous Coronary Interventionsmentioning

confidence: 99%

Troponin: the biomarker of choice for the detection of cardiac injury

Babuin¹

2005

Canadian Medical Association Journal

550

390

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T roponin is the biomarker of choice for the detection of cardiac injury. To use it properly, one must understand how sensitive the specific assay being used is for detecting cardiac injury, the fact that elevated troponin levels are highly specific for cardiac injury and some critical issues related to the basic science of the protein and its measurement. In this article, we review the biology of troponin, characteristics of assays that measure serum troponin levels and how to apply these measurements to patients who present with possible cardiovascular disease. We also discuss other clinical situations in which troponin levels may be elevated. The biology of troponinThe 3-unit troponin complex (troponin I, T and C) along with tropomyosin is located on the actin filament and is essential for the calcium-mediated regulation of skeletal and cardiac muscle contraction. 1 There are tissue-specific isoforms of troponin I, T and C. 2,3 Because the cardiac isoform of troponin C is shared by slow-twitch skeletal muscles, troponin C does not have cardiac specificity and thus is not used in assays for the diagnosis of cardiac injury. 4 There is one cardiac troponin I (cTnI) isoform in myocardial tissue. 5 This isoform has a post-translational tail of 32 amino acids on the N-terminus. 6,7 This sequence and the 42% and 45% dissimilarity with sequences of the other isoforms 8 have made possible the generation of highly specific monoclonal antibodies without cross-reactivity with other noncardiac forms. 9 Three genes control cardiac troponin T (cTnT). 10 These genes and alternative mRNA splicing produce a series of isoforms 10,11 with variable sequences close to the regions of the N-terminus and C-terminus. 10,12 Human cardiac muscle contains 4 troponin T isoforms, but only one is characteristic of the normal adult heart. 13,14 Highly specific antibodies have been made to the N-terminus-specific sequence of this cTnT isoform. 15 The skeletal isoforms present in the fetal heart are replaced by cTnI and cTnT late during fetal development. 16,17 cTnI is not expressed in skeletal muscle or other tissues during development 17 or in response to degenerative or regenerative muscle disease processes. 18 Thus, it is unlikely to be reexpressed in damaged tissues. The situation is more complex for cTnT. Re-expression of fetal forms occurs in cardiac tissue 12 and in diseased skeletal muscle. 19 With the firstgeneration cTnT assay, this problem was compounded by a nonspecific tag antibody that cross-reacted with troponin T in skeletal muscle. 20 Once this antibody was replaced by one with high specificity, false-positive elevations from skeletal muscle were eliminated. 15 Studies using immunohistochemistry and polymerase chain reaction have confirmed that these fetal isoforms are not detected by the assay used today. 21,22 Thus, the assay used to measure cTnT levels has cardiac specificity equivalent to that of assays for cTnI. Characteristics of troponin assaysMost troponin is found in the 3-unit complex (troponin I, T and C) of the c...

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“…Traditional biomarkers of myocardial necrosis, such as creatine kinase isoenzyme MB (CK-MB) and myoglobin are commonly increased in patients with chronic renal failure, even in the absence of clinically suspected myocardial ischemia (5,6). Moreover, cardiac biomarkers are more likely to be elevated in HD patients than in those with renal failure not on dialysis and their value should hence be interpreted with caution (7).…”

Section: Introductionmentioning

confidence: 99%

Effect of hemodialysis on traditional and innovative cardiac markers

Montagnana

Lippi

Tessitore

et al. 2008

Clinical Laboratory Analysis

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The diagnostic approach to acute coronary syndrome (ACS) is challenging in patients with impaired renal function since most serum biomarkers are commonly increased in this clinical setting. Cardiac troponin T (cTnT), creatine kinase isoenzyme MB (CK MB), myoglobin, and ischemia modified albumin (IMA), were assayed in 45 patients prehemodialysis (pre-HD) and posthemodialysis (post-HD), and results were adjusted for hemoconcentration. The pre-HD values of serum IMA and cTnT were above the respective diagnostic thresholds (IMAo85 K units/L; cTnT o0.03 ng/mL) in six (13%) and 27 (60%) patients undergoing chronic HD, respectively. A significant (105.0 vs. 79.0 K units/L, Po0.0001) and variable (138%; 95% confidence interval [CI], 12-65%) increase of serum IMA was observed post-HD, whereas the other biomarkers significantly decreased (cTnT: 0.029 vs. 0.044 ng/mL, P 5 0.016; CK-MB:2.33 vs.2.50 mg/L, Po 0.0001; myoglobin: 128.1 vs. 148.7 mg/L, Po0.0001). Biomarkers of myocardial injury, especially cTnT and IMA, might be used in HD patients, provided that an appropriate diagnostic interpretation is guarantee, according to individual baseine value, metabolism, and time of sampling. Moreover, IMA might be reliably applied to stratify the long-term risk of these patients, but not for diagnosing an ACS during or immediately post-HD.

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Creatine Kinase Subf orm Analysis in Hemodialysis Patients without Acute Coronary Syndromes

Cited by 24 publications

References 6 publications

Predictive markers of asymptomatic atherosclerosis in end-stage renal disease patients

Predictive markers of asymptomatic atherosclerosis in end-stage renal disease patients

Troponin: the biomarker of choice for the detection of cardiac injury

Effect of hemodialysis on traditional and innovative cardiac markers

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