Clinical findings in patients with cardiac troponin T elevation and end-stage renal disease without acute coronary syndrome

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.

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Cardiac Troponin T as a Prognostic Marker of Cardiovascular Morbidity and Mortality in Patients with End-stage Renal Disease

MGM Journal of Medical Sciences ◽

10.5005/jp-journals-10036-1120 ◽

2016 ◽

Vol 3 (4) ◽

pp. 176-180

Author(s):

Jaishree Ghanekar ◽

Asees P Singh ◽

Rohan Yewale

Keyword(s):

Renal Disease ◽

Prognostic Marker ◽

End Stage Renal Disease ◽

Cardiac Troponin ◽

Troponin T ◽

Cardiovascular Morbidity ◽

Cardiac Troponin T ◽

Cardiovascular Morbidity And Mortality ◽

Stage Renal Disease ◽

End Stage

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

Clinical Chemistry ◽

10.1373/clinchem.2016.261644 ◽

2017 ◽

Vol 63 (3) ◽

pp. 683-690 ◽

Cited By ~ 20

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.

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