scholarly journals Cardiac Troponin T: Smaller Molecules in Patients with End-Stage Renal Disease than after Onset of Acute Myocardial Infarction

2017 ◽  
Vol 63 (3) ◽  
pp. 683-690 ◽  
Author(s):  
Alma M A Mingels ◽  
Eline P M Cardinaels ◽  
Natascha J H Broers ◽  
Anneke van Sleeuwen ◽  
Alexander S Streng ◽  
...  

Abstract BACKGROUND We have found previously that in acute myocardial infarction (AMI), cardiac troponin T (cTnT) is degraded in a time-dependent pattern. We investigated whether cTnT forms differed in patients with chronic cTnT increases, as seen with renal dysfunction, from those in the acute phase of myocardial infarction. METHODS We separated cTnT forms by gel filtration chromatography (GFC) in end-stage renal disease (ESRD) patients: prehemodialysis (pre-HD) and post-HD (n = 10) and 2 months follow-up (n = 6). Purified (cTnT) standards, quality control materials of the clinical cTnT immunoassay (Roche), and AMI patients' sera also were analyzed. Immunoprecipitation and Western blotting were performed with the original cTnT antibodies from the clinical assay and antibodies against the N- and C-terminal end of cTnT. RESULTS GFC analysis revealed the retention of purified cTnT at 27.5 mL, identical to that for cTnT in quality controls. For all ESRD patients, one cTnT peak was found at 45 mL, pre- and post-HD, and stable over time. Western blotting illustrated that this peak corresponded to cTnT fragments <18 kDa missing the N- and C-terminal ends. AMI patients' sera revealed cTnT peaks at 27.5 and 45 mL, respectively, corresponding to N-terminal truncated cTnT of 29 kDa and N- and C-terminal truncated fragments of <18 kDa, respectively. CONCLUSIONS We found that cTnT forms in ESRD patients are small (<18 kDa) and different from forms seen in AMI patients. These insights may prove useful for development of a more specific cTnT immunoassay, especially for the acute and diagnostic phase of myocardial infarction.

Circulation ◽  
2020 ◽  
Vol 142 (Suppl_3) ◽  
Author(s):  
Vikram Sharma ◽  
Ruchi Sharma ◽  
Shehab A Alansari ◽  
Mohan L Maradumane ◽  
Conner P Witherow ◽  
...  

Introduction: Circulating blood troponin complexes and free fractions remain poorly characterised in different conditions where troponin is detectable in blood Hypothesis: The aim of the study was to compare the differences in troponin-I(TnI) complexes/free-forms in end stage renal disease (ESRD) compared to acute myocardial infarction(AMI) Methods: Blood was collected from patients with AMI(n=7) or ESRD(n=4) at two time points (a)As early as possible after AMI or at initial contact with ESRD patients and (b)24-48 hours later. Western blotting was carried out with HyTest cTnI-560cc antibody on plasma extracted from whole blood. Densitometry analysis was performed and evaluated using the independent samples T-test and paired T-test as appropriate Results: Prominent bands were noted at ~45,~37 and ~25 kDa respectively representing low molecular weight(LMW) TnI-TnT-TnC complex, binary TnI-TnC complex and free-TnI. At time-point (a), there was no difference in these bands between STEMI and CKD patients. Interestingly, at time-point (b), AMI patients had significantly lower intensity of the 45kDa and 37kDa bands compared to CKD patients(for 45 kDa band mean difference was 54.3±19.4 AU, p=0.02; for 37 kDa band mean difference was 27.7±10.5 AU, p=0.03) as well as compared to the initial STEMI samples taken at time-point (a)(for 45 kDa band mean difference was 41.4±8.1 AU, p=0.002; for 37 kDa band mean difference was 16.7±6.3 AU, p=0.002) ,however there was no difference in the 25kDa band Conclusions: AMI patients had progressively lesser quantities of circulating LMW-ITC and binary IC complexes following AMI compared to ESRD patients, but similar quantities of circulating free TnI. This indicates a constant release of LMW-ITC and binary-IC complexes from the myocardium or reduced glomerular filtration of these complexes in ESRD while in the AMI patients, the LMW-ITC and binary I-C complexes appear to be progressively eliminated from plasma after the initial release


2021 ◽  
Vol 28 (5) ◽  
pp. 64-71
Author(s):  
Wan Nur Aimi Wan Mohd Zamri ◽  
◽  
Noorazliyana Shafii ◽  
Tuan Salwani Tuan Ismail ◽  
Adlin Zafrulan Zakaria ◽  
...  

Background: In end-stage renal disease (ESRD), troponin T concentrations can be elevated even without cardiac ischaemia, which hampers the diagnosis of acute myocardial infarction (AMI). The objectives of our study were to determine the proportion of dialysisdependent ESRD patients without acute coronary syndrome (ACS) but with highly sensitive cardiac troponin T (hs-cTnT) levels above the 99th percentile upper reference limit and to evaluate the range of hs-cTnT among this population. Methods: A cross-sectional study was conducted at the haemodialysis (HD) unit of a tertiary hospital in Malaysia from January 2018 to February 2019. Dialysis-dependent ESRD patients were included and those with a recent history of ACS (within 30 days) were excluded. Pre-dialysed serum hs-cTnT levels were measured using Cobas e411. The upper limit of the 99th percentile value for troponin T was 14 ng/L. Results: A total of 150 patients were recruited as study participants. The majority were female (62%) and of Malay ethnicity (94%), and the mean (SD) age was 45.19 (16.36) years old. The hs-cTnT range (min, max) was 11.39–738.30 ng/L and the median (interquartile range [IQR]) of hs-cTnT was 59.20 (83.41) ng/L. Elevated hs-cTnT levels were observed in 149/150 (99%) of the study participants (54/55 [98.2%] of the patients were on HD, and 95/95 [100.0%] of the patients were on continuous ambulatory peritoneal dialysis). Conclusion: This study supports prior research showing that even without ACS, most ESRD patients have elevated concentrations of cardiac troponin. Furthermore, our study illustrates the need to revisit the use of absolute troponin values when making a diagnosis of ACS in ESRD patients.


1995 ◽  
Vol 41 (8) ◽  
pp. 1202-1203 ◽  
Author(s):  
Gerd Hafner ◽  
Birgit Thome-Kromer ◽  
Johannes Schaube ◽  
Iri Kupferwasser ◽  
Wolfram Ehrenthal ◽  
...  

1995 ◽  
Vol 41 (8) ◽  
pp. 1201-1202 ◽  
Author(s):  
H A Katus ◽  
C Haller ◽  
M Müller-Bardorff ◽  
T Scheffold ◽  
A Remppis

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