scholarly journals Cardiac Troponin T Is Elevated in Asymptomatic Patients With Chronic Renal Failure

1996 ◽  
Vol 106 (1) ◽  
pp. 118-123 ◽  
Author(s):  
Wendy L. Frankel ◽  
David A. Herold ◽  
Thomas W. Ziegler ◽  
Robert L. Fitzgerald
1998 ◽  
Vol 270 (2) ◽  
pp. 183-188 ◽  
Author(s):  
Junnichi Ishii ◽  
Takashi Ishikawa ◽  
Junn Yukitake ◽  
Youichi Nagamura ◽  
Mikiya Ito ◽  
...  

2019 ◽  
Vol 132 (5) ◽  
pp. 631-638
Author(s):  
Diego Martín Raymondi ◽  
Héctor Garcia ◽  
Isabel Álvarez ◽  
Luis Hernández ◽  
Jorge Palazuelos Molinero ◽  
...  

2001 ◽  
Vol 47 (6) ◽  
pp. 1023-1030 ◽  
Author(s):  
Salim Fredericks ◽  
Joanne F Murray ◽  
Michael Bewick ◽  
René Chang ◽  
Paul O Collinson ◽  
...  

Abstract Background: Serum cardiac troponin T (cTnT) concentrations may be increased in patients with renal dysfunction without evidence of cardiac damage, as assessed by conventional methods. It has been suggested that these positive measurements result from the expression in skeletal muscle of fetal isoforms of cTnT, which are detected by the cTnT immunoassay. Methods: Skeletal muscle (exterior oblique) biopsies were taken from healthy living kidney donors (n = 5) and transplant recipients (n = 19). The amounts of cTnT and creatine kinase (CK) isoenzymes in skeletal muscle of healthy controls were compared with those in patients with renal failure (Wilcoxon–Mann–Whitney test). cTnT was measured quantitatively by a second-generation assay, with a limit of detection of 1 μg/g of protein, and qualitatively by immunohistochemistry and immunoblotting. CK-MB was measured by quantitative electrophoresis. Results: Minute quantities of cTnT were detected in 2 of the 5 (40%) control samples and 9 of the 19 (47%) renal failure samples, respectively, at mean concentrations of <5 μg/g of protein for both subject groups. This was <1/6000th that found in heart muscle. There was no significant difference in cTnT or CK-MB content in skeletal muscle between healthy controls and patients with renal failure. Increased serum cTnT did not predict detectable cTnT in skeletal muscle. cTnT was not detected qualitatively by immunoblotting or immunohistochemistry in any skeletal muscle samples. Conclusions: Uremia does not affect the content of cTnT or CK-MB in exterior oblique muscle, suggesting that cTnT detected in serum from patients with renal failure does not originate from skeletal muscle.


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.


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