scholarly journals Elevation of Highly Sensitive Cardiac Troponin T Among End-Stage Renal Disease Patients Without Acute Coronary Syndrome

2021 ◽  
Vol 28 (5) ◽  
pp. 64-71
Author(s):  
Wan Nur Aimi Wan Mohd Zamri ◽  
◽  
Noorazliyana Shafii ◽  
Tuan Salwani Tuan Ismail ◽  
Adlin Zafrulan Zakaria ◽  
...  
Keyword(s):  
End Stage Renal Disease ◽  
Cardiac Troponin ◽  
Troponin T ◽  
Cardiac Troponin T ◽  
Coronary Syndrome ◽  
Highly Sensitive ◽  
Stage Renal Disease ◽  
End Stage ◽  
Study Participants ◽  
Esrd Patients

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.

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 ◽  
...  
Keyword(s):  
Myocardial Infarction ◽  
Acute Myocardial Infarction ◽  
Renal Disease ◽  
End Stage Renal Disease ◽  
Cardiac Troponin ◽  
Troponin T ◽  
Cardiac Troponin T ◽  
Stage Renal Disease ◽  
End Stage ◽  
Esrd Patients

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.

scholarly journals Multi-Biomarker Risk Stratification of N-Terminal Pro-B-Type Natriuretic Peptide, High-Sensitivity C-Reactive Protein, and Cardiac Troponin T and I in End-Stage Renal Disease for All-Cause Death

2004 ◽  
Vol 50 (12) ◽  
pp. 2279-2285 ◽  
Author(s):  
Fred S Apple ◽  
MaryAnn M Murakami ◽  
Lesly A Pearce ◽  
Charles A Herzog
Keyword(s):  
End Stage Renal Disease ◽  
Cardiac Troponin ◽  
Troponin T ◽  
High Sensitivity ◽  
C Reactive Protein ◽  
Reactive Protein ◽  
Multiple Biomarkers ◽  
Stage Renal Disease ◽  
End Stage ◽  
Esrd Patients

Abstract Background: In patients with end-stage renal disease (ESRD), the ability of single and multiple biomarker monitoring to predict adverse outcomes has not been well established. This study determined the prognostic value of multiple biomarkers for all-cause death over 2 years in 399 ESRD patients. Methods: The risk of all-cause death was determined by use of multiple biomarkers based on concentrations for a reference population (normal) and cutoffs based on tertile distributions in the ESRD group. Biomarkers studied included N-terminal pro-B-type natriuretic peptide (NT-proBNP), high-sensitivity C-reactive protein (hsCRP; Dade Behring and Roche assays), and cardiac troponin T (cTnT; Roche) and I (cTnI; Dade Behring and Beckman Coulter assays). Relative risks of death were estimated and survival curves computed. Results: A total of 101 deaths occurred during 594 patient-years of follow-up. Increased NT-proBNP concentrations were not predictive of death on the basis of the normal cutoffs. However, tertile analysis of NT-proBNP was significantly predictive of death and had a ROC area under the curve equivalent to or better than any of the other biomarkers. Biomarkers independently predictive of survival were hsCRP (P <0.001, either assay), cTnT (P <0.05), and cTnI (Dade, P <0.05). Two-year mortality rates were 6% (n = 45) with normal hsCRP, cTnI, and cTnT concentrations; 19% (n = 173) with increased hsCRP or cTnT and normal cTnI; 44% (n = 160) with both hsCRP and cTnT increased and normal cTnI; 61% (n = 21) with increased cTnI (Dade) or 47% (n = 74) with increased cTnI (Beckman) regardless of hsCRP or cTnT concentrations. Defined by the normal cutoffs, increased concentrations of biomarkers were present in various proportions of the 399 patients with ESRD: NT-proBNP, 99%; hsCRP, 46% (both Roche and Dade assays); cTnT, 85%; cTnI, 19% (Beckman assay) and 5% (Dade assay). Conclusions: Although mechanisms likely vary for causation, increased plasma hsCRP, cTnT, and cTnI above the cutoffs for our reference (normal) population were all independently predictive of subsequent death in ESRD patients. Tertile analysis for NT-proBNP also demonstrated prognostic value.

scholarly journals Cardiac troponin T in patients with end-stage renal disease: absence of expression in truncal skeletal muscle

1998 ◽  
Vol 44 (5) ◽  
pp. 930-938 ◽  
Author(s):  
Christlieb Haller ◽  
Jörg Zehelein ◽  
Andrew Remppis ◽  
Margit Müller-Bardorff ◽  
Hugo A Katus
Keyword(s):  
Skeletal Muscle ◽  
Coronary Artery Disease ◽  
Coronary Artery ◽  
End Stage Renal Disease ◽  
Cardiac Troponin ◽  
Troponin T ◽  
Cardiac Troponin T ◽  
Artery Disease ◽  
Stage Renal Disease ◽  
End Stage

Abstract In patients with end-stage renal disease (ESRD), the serum concentration of cardiac troponin T (cTnT) may be increased without cardiac ischemia. One reason for this unexplained increase could be the extracardiac expression of cTnT. However, truncal skeletal muscle biopsies of five patients with ESRD showed no evidence of the expression of either cTnT mRNA (reverse transcription-PCR) or protein (immunoblot, immunofluorescence). We also measured the serum concentration of cTnT in 97 patients with ESRD. The serum cTnT concentration determined in both first and second generation cTnT assays was significantly lower P <0.01 in patients with a low cardiac risk than in patients with positive indicators of coronary artery disease. The correlation between cTnT and indicators of coronary artery disease is consistent with the hypothesis that cTnT in the serum of patients with ESRD originates from the heart.

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