scholarly journals Cardiac Troponins in Patients with Renal Dysfunction

Author(s):  
P O Collinson ◽  
L Hadcocks ◽  
Y Foo ◽  
S B Rosalki ◽  
P J Stubbs ◽  
...  

Cardiac troponin T (cTnT) and cardiac troponin I (cTnI) were measured in 198 patients with renal dysfunction [132 men: median (range) age 66·1 (8·2-90·3) years]. cTnT was measured by two methods: ELISA and Enzymun (Boehringer Mannheim UK, Lewes, UK), both with a detection limit of 0·05 μg/L in 179 and 78 patients, respectively. cTnI was measured in 80 patients by the OPUS plus and OPUS Magnum systems (Dade-Behring, Milton Keynes, UK) with a detection limit of 0·5 μg/L. Patients were classified as having chronic renal impairment (CRI), chronic renal failure (CRF), acute renal failure including those with multiple organ failure on renal replacement therapy (ARF), and patients with chronic renal failure treated with haemodialysis (HD). Cardiac troponins were detectable in the serum of patients with renal dysfunction. cTnT was detectable in 113/179 (63·1%) and 33/78 (42·3%) by the ELISA and Enzymun methods respectively. cTnI was detectable in 17/80 (21·3%). cTnT (ELISA and Enzymun methods) and cTnI were detectable with increased frequency in the CRF, HD and ARF patient groups compared with the CRI group. Cardiac troponin concentrations did not correlate with serum creatine kinase (CK) activity, CK-MB, or urea or creatinine levels. Serial cardiac troponin measurements may be required to confirm or exclude a diagnosis of acute coronary syndromes in patients with renal dysfunction.

Author(s):  
Giuseppe Lippi ◽  
Fabian Sanchis-Gomar ◽  
Gianfranco Cervellin

AbstractBackground:The pathogenesis of different types of myocardial infarction (MI) differs widely, so that accurate and timely differential diagnosis is essential for tailoring treatments according to the underlying causal mechanisms. As the measurement of cardiac troponins is a mainstay for diagnosis and management of MI, we performed a systematic literature analysis of published works which concomitantly measured cardiac troponins in type 1 and 2 MI.Methods:The electronic search was conducted in Medline, Scopus and Web of Science using the keywords “myocardial infarction” AND “type(-)2” OR “type II” AND “troponin” in “Title/Abstract/Keywords”, with no language restriction and date limited from 2007 to the present.Results:Overall, 103 documents were identified, but 95 were excluded as precise comparison of troponin values in patients with type 1 and 2 MI was unavailable. Therefore, eight studies were finally selected for our analysis. Two studies used high-sensitivity (HS) immunoassays for measuring cardiac troponin T (HS-TnT), one used a HS immunoassay for measuring cardiac troponin I (HS-TnI), whereas the remaining used conventional methods for measuring TnI. In all studies, regardless of type and assay sensitivity, troponin values were higher in type 1 than in type 2 MI. The weighted percentage difference between type 1 and 2 MI was 32% for TnT and 91% for TnI, respectively. Post-discharge mortality obtained from pooling individual data was instead three times higher in type 2 than in type 1 MI.Conclusions:The results of our analysis suggest that the value of cardiac troponins is consistently higher in type 1 than in type 2 MI.


2019 ◽  
Vol 20 (11) ◽  
pp. 2638 ◽  
Author(s):  
Michaela Adamcova ◽  
Veronika Skarkova ◽  
Jitka Seifertova ◽  
Emil Rudolf

Modern diagnostic strategies for early recognition of cancer therapeutics-related cardiac dysfunction involve cardiac troponins measurement. Still, the role of other markers of cardiotoxicity is still unclear. The present study was designed to investigate dynamics of response of human cardiomyocytes derived from induced pluripotent stem cells (hiPCS-CMs) to doxorubicin with the special emphasis on their morphological changes in relation to expression and organization of troponins. The hiPCS-CMs were treated with doxorubicin concentrations (1 and 0.3 µM) for 48 h and followed for next up to 6 days. Exposure of hiPCS-CMs to 1 µM doxorubicininduced suppression of both cardiac troponin T (cTnT) and cardiac troponin I (cTnI) gene expression. Conversely, lower 0.3 µM doxorubicin concentration produced no significant changes in the expression of aforementioned genes. However, the intracellular topography, arrangement, and abundance of cardiac troponin proteins markedly changed after both doxorubicin concentrations. In particular, at 48 h of treatment, both cTnT and cTnI bundles started to reorganize, with some of them forming compacted shapes extending outwards and protruding outside the cells. At later intervals (72 h and onwards), the whole troponin network collapsed and became highly disorganized following, to some degree, overall changes in the cellular shape. Moreover, membrane permeability of cardiomyocytes was increased, and intracellular mitochondrial network rearranged and hypofunctional. Together, our results demonstrate complex effects of clinically relevant doxorubicin concentrations on hiPCS-CM cells including changes in cTnT and cTnI, but also in other cellular compartments contributing to the overall cytotoxicity of this class of cytostatics.


2020 ◽  
Vol 154 (Supplement_1) ◽  
pp. S89-S90
Author(s):  
J M Rohr ◽  
S Pirruccello ◽  
A Sofronescu

Abstract Introduction/Objective Serial cardiac troponin measurement is a sensitive method to identify recent cardiac injury and is a necessary function of the clinical chemistry laboratory. We present a case of out-of-range cardiac troponin I (cTnI) elevation which remained spuriously elevated for at least 30 days. Methods Cardiac troponins were measured on a DxI (Beckman Coulter), Vitros 5600 (Ortho Clinical Diagnostics), iSTAT (Abbott), and Cobas e602 (Roche) according to the manufacturers’ instructions with appropriate controls. Heterophile antibody blocking (Scantibodies Laboratories) was performed according to the package insert. Results A 58-year-old male with a medical history significant for chronic non-ischemic cardiomyopathy with open valvular repair (ejection fraction 15-20%), chronic atrial fibrillation, and Hodgkin’s lymphoma in remission presented to a rural clinic with chest pain and a cTnI of 0.8 ng/mL (reference <0.04 ng/mL). He was transferred to our tertiary center for open revision. The patient’s cTnI (measured on a Beckman Coulter DxI) was above linearity threshold (>71.00 ng/mL) starting day 1 after surgery. The patient self-discharged against medical advice on day 16. On day 21 he experienced new chest pain and dyspnea and was readmitted with a cardiac troponin T (cTnT) of >35 ng/mL (iSTAT; reference <0.08 ng/mL) and cTnI again above threshold. This value remained elevated for the next five days despite abated symptoms. To address the discordant laboratory and physical findings, dilutional cTnI measurements on serum from day 30 demonstrated linearity. Heterophile antibody testing was negative. cTnI on the DxI machine remained >71.00 ng/mL but was separately measured as 3.4 ng/mL (Vitros 5600, reference <0.08 ng/mL). cTnT was found to be 1.05 ng/mL (Cobas e602; reference 0.00 ng/mL). Comparative examination of all methodologies was unrevealing. Conclusion This case demonstrates a spurious elevation of cardiac troponins which remarkably demonstrated linearity on serial dilution. Multiple testing methodologies were necessary to prove fallacy. The cause of the result remains unclear. The clinical pathologist should be aware of possible false positives and investigate unlikely continuous cardiac troponin elevations.


2003 ◽  
Vol 98 (4) ◽  
pp. 188-192 ◽  
Author(s):  
Dirk Peetz ◽  
Sabina Sch�tt ◽  
Bernd Suck� ◽  
Andreas Faldum ◽  
Evelyn Wandel ◽  
...  

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