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

Alma M. A. Mingels; Eline P. M. Cardinaels; Natascha J. H. Broers; Anneke van Sleeuwen; Alexander S. Streng; Marja P. van Dieijen-Visser; Jeroen P. Kooman; Otto Bekers

doi:10.1373/clinchem.2016.261644

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

Alma M. A. Mingels^*, Eline P. M. Cardinaels, Natascha J. H. Broers, Anneke van Sleeuwen, Alexander S. Streng, Marja P. van Dieijen-Visser, Jeroen P. Kooman, Otto Bekers

^*Corresponding author for this work

Research output: Contribution to journal › Article › Academic › peer-review

26 Citations (Web of Science)

6 Downloads (Pure)

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

CONCLUSIONS: We found that cTnT forms in ESRD patients are small (

Original language	English
Pages (from-to)	683-690
Number of pages	8
Journal	Clinical Chemistry
Volume	63
Issue number	3
DOIs	https://doi.org/10.1373/clinchem.2016.261644
Publication status	Published - Mar 2017

Keywords

ACUTE CORONARY SYNDROME
HIGH-SENSITIVITY
HEMODIALYSIS-PATIENTS
HEART-FAILURE
DEGRADATION
ASSAYS
ASSOCIATION
POPULATION
CHALLENGES
MORTALITY

Access to Document

10.1373/clinchem.2016.261644

Full text Final published version, 874 KBLicence: Taverne

Cite this

@article{629d33c31f164bf88e6b2ad4199cf537,

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

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 fragmentsCONCLUSIONS: We found that cTnT forms in ESRD patients are small (",

keywords = "ACUTE CORONARY SYNDROME, HIGH-SENSITIVITY, HEMODIALYSIS-PATIENTS, HEART-FAILURE, DEGRADATION, ASSAYS, ASSOCIATION, POPULATION, CHALLENGES, MORTALITY",

author = "Mingels, {Alma M. A.} and Cardinaels, {Eline P. M.} and Broers, {Natascha J. H.} and {van Sleeuwen}, Anneke and Streng, {Alexander S.} and {van Dieijen-Visser}, {Marja P.} and Kooman, {Jeroen P.} and Otto Bekers",

year = "2017",

month = mar,

doi = "10.1373/clinchem.2016.261644",

language = "English",

volume = "63",

pages = "683--690",

journal = "Clinical Chemistry",

issn = "0009-9147",

publisher = "American Association for Clinical Chemistry",

number = "3",

}

TY - JOUR

T1 - Cardiac Troponin T

T2 - Smaller Molecules in Patients with End-Stage Renal Disease than after Onset of Acute Myocardial Infarction

AU - Mingels, Alma M. A.

AU - Cardinaels, Eline P. M.

AU - Broers, Natascha J. H.

AU - van Sleeuwen, Anneke

AU - Streng, Alexander S.

AU - van Dieijen-Visser, Marja P.

AU - Kooman, Jeroen P.

AU - Bekers, Otto

PY - 2017/3

Y1 - 2017/3

N2 - 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 fragmentsCONCLUSIONS: We found that cTnT forms in ESRD patients are small (

AB - 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 fragmentsCONCLUSIONS: We found that cTnT forms in ESRD patients are small (

KW - ACUTE CORONARY SYNDROME

KW - HIGH-SENSITIVITY

KW - HEMODIALYSIS-PATIENTS

KW - HEART-FAILURE

KW - DEGRADATION

KW - ASSAYS

KW - ASSOCIATION

KW - POPULATION

KW - CHALLENGES

KW - MORTALITY

U2 - 10.1373/clinchem.2016.261644

DO - 10.1373/clinchem.2016.261644

M3 - Article

C2 - 28073901

VL - 63

SP - 683

EP - 690

JO - Clinical Chemistry

JF - Clinical Chemistry

SN - 0009-9147

IS - 3

ER -