Evaluation of Cardiac Troponin T Elevation in Patients with Chronic Renal Failure Undergoing Dialysis

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.

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Cardiac Troponins in Patients with Renal Dysfunction

Annals of Clinical Biochemistry International Journal of Laboratory Medicine ◽

10.1177/000456329803500306 ◽

1998 ◽

Vol 35 (3) ◽

pp. 380-386 ◽

Cited By ~ 68

Author(s):

P O Collinson ◽

L Hadcocks ◽

Y Foo ◽

S B Rosalki ◽

P J Stubbs ◽

...

Keyword(s):

Renal Failure ◽

Chronic Renal Failure ◽

Detection Limit ◽

Renal Dysfunction ◽

Cardiac Troponin ◽

Troponin I ◽

Troponin T ◽

Multiple Organ ◽

Chronic Renal Impairment ◽

Cardiac Troponins

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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High-NaCl Diet Aggravates Cardiac Injury in Rats with Adenine-Induced Chronic Renal Failure and Increases Serum Troponin T Levels

Cardiorenal Medicine ◽

10.1159/000446547 ◽

2016 ◽

Vol 6 (4) ◽

pp. 317-327 ◽

Cited By ~ 3

Author(s):

Pavlos Kashioulis ◽

Ola Hammarsten ◽

Niels Marcussen ◽

Emman Shubbar ◽

Aso Saeed ◽

...

Keyword(s):

Renal Failure ◽

Chronic Renal Failure ◽

Cardiac Troponin ◽

Troponin T ◽

Cardiac Injury ◽

Serum Levels ◽

Left Ventricular ◽

Sprague Dawley ◽

Small Artery ◽

Sprague Dawley Rats

Aims: To examine the effects of 2 weeks of high-NaCl diet on left ventricular (LV) morphology and serum levels of cardiac troponin T (cTnT) in rats with adenine-induced chronic renal failure (ACRF). Methods: Male Sprague-Dawley rats either received chow containing adenine or were pair-fed an identical diet without adenine [controls (C)]. Approximately 10 weeks after the beginning of the study, the rats were randomized to either remain on a normal NaCl diet (NNa; 0.6%) or to be switched to high-NaCl chow (HNa; 4%) for 2 weeks, after which acute experiments were performed. Results: Rats with ACRF showed statistically significant increases (p < 0.001) in arterial pressure (AP), LV weight and fibrosis, and serum cTnT levels compared to controls. Two weeks of high-NaCl intake augmented the increases in AP, LV weight and fibrosis, and serum cTnT concentrations only in ACRF rats (p < 0.05 for group × NaCl intake interaction). Compared to group C-NNa, cTnT levels were elevated approximately 6-fold in group ACRF-NNa and 24-fold in group ACRF-HNa. Focal LV injury with cardiomyocyte necrosis, scarring, and fibrinoid necrosis of small arteries were only detected in group ACRF-HNa. There was a strong correlation between the degree of LV fibrosis and serum cTnT levels in ACRF rats (r = 0.81, p < 0.01). Conclusion: Two weeks of high-NaCl diet in rats with ACRF produces LV injury and aggravates increases in serum cTnT levels, presumably by causing hypertension-induced small artery lesions leading to myocardial ischemia. This model may be suitable for studying pathophysiological mechanisms in chronic renicardiac syndromes.

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Cardiac Troponin T and I in End-Stage Renal Failure

Clinical Chemistry ◽

10.1093/clinchem/46.9.1345 ◽

2000 ◽

Vol 46 (9) ◽

pp. 1345-1350 ◽

Cited By ~ 102

Author(s):

Diana Wayand ◽

Hannsjörg Baum ◽

Gabriele Schätzle ◽

Julia Schärf ◽

Dieter Neumeier

Keyword(s):

Renal Failure ◽

Cardiac Troponin ◽

Troponin T ◽

Cardiac Complications ◽

Cardiac Troponin T ◽

End Stage Renal Failure ◽

History Of ◽

Group 2 ◽

End Stage ◽

Group 1

Abstract Background: In patients suffering from end-stage renal failure, cardiac troponin T (cTnT) and I (cTnI) may be increased in serum without other signs of acute myocardial damage. Whether these increases are specific to myocardial injury or nonspecific is not completely clear. Methods: We investigated time courses of cTnT and cTnI over 1 year and the clinical outcome over 2 years in 59 patients with end-stage renal failure undergoing chronic hemodialysis. At the start of the study, we divided the patients into two groups, group 1, without history of cardiac failure, and group 2, with history of cardiac failure, and looked for differences between the groups in later adverse outcome. cTnT was measured using the Enzymun® troponin T assay on an ES 700 analyzer (Roche). cTnI was measured on a Stratus® II analyzer (Dade Behring). Creatinine and blood urea nitrogen were measured on a Vitros® 950 IRC (Ortho). Results: Dialysis acutely increased cTnT (P <0.01) and decreased cTnI (P <0.001) regardless of the dialysis membrane used. Although statistically not significant, cTnT but not cTnI was increased more frequently in group 2 than in group 1, in some cases over the whole study period. Five patients (8.5%) died of cardiac complications within 2 years; all of them had mostly increased cTnT and, in one or more samples, increased cTnI. Conclusions: Dialysis alters measured cTnT and cTnI concentrations in serum. In patients suffering from end-stage renal failure, sporadic or persistently increased cTnT and cTnI appear to predict cardiac complications. Because of the effects of the dialysis procedure on troponin values, we recommend that blood be collected before dialysis.

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