Factors associated with increased serum levels of cardiac troponins T and I in chronic haemodialysis patients: Chronic Haemodialysis And New Cardiac Markers Evaluation (CHANCE) study

Iliou, Marie Christine; Fumeron, Christine; Benoit, Marie-Odile; Tuppin, Philippe; Courvoisier, Claire Le; Calonge, Victorio Menoyo; Moatti, N.; Buisson, Claude; Jacquot, C.

doi:10.1093/ndt/16.7.1452

Cited by 101 publications

(96 citation statements)

References 18 publications

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“…By contrast, cTnI was only increased (50.6 mg/L) in 0.4% of their patients. Iliou et al 50 observed cTnT concentrations 40.1 mg/L in 19% of 258 haemodialysis patients; only 2% demonstrated elevated concentrations of cTnI. Left ventricular mass was associated with cTnT, but not cTnI, concentration, and it has been suggested 49 that LVH may explain the di¡ering behaviour of these markers in haemodialysis patients, with a di¡erent release pattern of cTnT compared to cTnI.…”

Section: Prevalence and Clinical Correlates Of Raised Serum Troponin mentioning

confidence: 99%

The significance of serum troponin T in patients with kidney disease: a review of the literature

2004

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The last 10 years have witnessed radical changes in the de nition and diagnosis of the acute coronary syndrome (ACS), including myocardial infarction, as a result of the introduction of sensitive and speci c markers of myocardial damage, the cardiac troponins. One barrier to the universal acceptance of these markers has been the observation that troponin T (cTnT) concentration is commonly increased in the presence of renal failure. Initially it was believed that this constituted an important false positive limitation of the test. This was confounded by problems with the initial cTnT assay and by the observation that troponin I (cTnI) was generally not increased in these patients. However, it has recently been demonstrated that the prognostic signi cance of a raised cTnT concentration in patients with a suspected ACS is unaffected by renal impairment. Further, powerful outcome studies are now being reported demonstrating that raised concentrations of serum cTnT are predictive of mortality in haemodialysis patients. This review summarizes our current understanding of the prevalence and signi cance of raised serum cTnT concentrations in patients with kidney disease and highlights areas where our understanding is incomplete. Evidence suggests that raised troponin concentrations in uraemic patients do indeed re ect myocardial injury. In the future, patients demonstrating this abnormality may be the target for more aggressive cardiac intervention, the advantages of which have been demonstrated in the non-uraemic population.

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Section: Prevalence and Clinical Correlates Of Raised Serum Troponin mentioning

confidence: 99%

The significance of serum troponin T in patients with kidney disease: a review of the literature

2004

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“…We speculate as to the possible causes for the difference in increases in cTnT compared with cTnI. First, increased cTnT but not cTnI reflects increased left ventricular mass in the ESRD population, 26,27 with a different release pattern of cTnT compared with cTnI. Second, cTnT release from injured myocardium may have a longer circulating half-life compared with cTnI because of advanced glycation end products known to accumulate in diabetic patients with renal disease.…”

Section: Apple Et Al Prognostic Value Of Troponin In Renal Disease 2943mentioning

confidence: 96%

Predictive Value of Cardiac Troponin I and T for Subsequent Death in End-Stage Renal Disease

et al. 2002

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Background-This study determined the prevalence of increased cardiac troponin I (cTnI) and T (cTnT) in end-stage renal disease (ESRD) patients and whether an increased troponin was predictive of death. Methods and Results-Serum was obtained from 733 ESRD patients and measured for cTnI and cTnT. Relative risks were estimated using Cox proportional hazards regressions univariately and adjusted for age, time on dialysis, and coronary artery disease. Kaplan-Meier curves compared time to event data between groups. Greater percentages of patients had an increased cTnT versus cTnI at each cutoff, as follows: 99th percentile, 82% versus 6%; 10% coefficient of variation, 53% versus 1.0%; and receiver operator characteristic, 20% versus 0.4%. Increased versus normal cTnT was predictive of increased mortality using all cutoffs and only above the 99th percentile for cTnI. Two-year cumulative mortality rates increased (PϽ0.001) with changes in cTnT from normal (Ͻ0.01 g/L, 8.4%) to small (Ն0.01 to Ͻ0.04 g/L, 26%), moderate (Ն0.04 to Ͻ0.1 g/L, 39%), and large (Ն0.1 g/L, 47%) increases. Two-year mortalities were 30% for cTnI Ͻ0.1 g/L and 52% if Ն0.1 g/L. Univariate and adjusted relative risks of death associated with elevated (Ͼ99th percentile) cTnT were 5.0 (CI, 2.5 to 10; PϽ0.001) and 3.9 (CI, 1.9 to7.9; PϽ0.001) and cTnI were 2.0 (CI, 1.3 to 3.3; Pϭ0.008) and 2.1 (CI, 1.3 to 3.3; Pϭ0.007). Age, coronary artery disease, and time on dialysis were also independent predictors of mortality. Conclusions-Increases in cTnT and cTnI in ESRD patients show a 2-to 5-fold increase in mortality, with a greater number of patients having an increased cTnT.

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“…Una possibile spiegazione è che possano rappresentare, almeno in parte, un danno miocardico subclinico, una risposta infiammatoria al danno cronico renale o a uno stato cronico di sovraccarico di volume a livello cardiaco 56 . La maggior parte degli studi è focalizzata su pazienti emodializzati, nei quali un aumento della troponina è associato all'età, alla concomitante presenza di fattori di rischio cardiovascolare, a una storia di malattia ischemica cardiaca, a diabete e a ipertensione ventricolare sinistra [57][58][59] . Aumentati livelli di troponina nei pazienti sottoposti a emodialisi da lungo tempo sembrerebbero correlare con la mortalità, non solo di natura cardiaca [59][60][61][62][63][64][65] .…”

Section: Cause DI Elevazione Delle Troponine Nel Danno Cardiaco Non Iunclassified

Cardiospecific troponins in non-ischemic cardiological pathologies

2006

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Materiale protetto da copyright. Non fotocopiare o distribuire elettronicamente senza l'autorizzazione scritta dell'editore. Struttura e meccanismo di rilascio delle troponineLe troponine cardiache sono proteine regolatrici che controllano l'interazione calcio-mediata di actina e miosina. Il complesso troponinico consta di 3 subunità: troponina T (TnT), che si lega alla tropomiosina e facilita la contrazione, troponina I (TnI), che si lega all'actina e inibisce l'interazione actina-miosina mediante inibizione dell'attività ATPasica dell'actomiosina e troponina C (TnC), che lega gli ioni calcio 1 . Nei filamenti sottili della fibra muscolare, sette monomeri di actina interagiscono con un dimero di tropomiosina e un complesso troponinico. Lo scivolamento di filamenti contigui garantisce la contrazione alla base della funzione motoria delle cellule muscolari. All'interno del miocita la TnT si trova prevalentemente in forma legata al TnC e TnI (complesso ternario T-I-C), ma ne esiste anche una forma libera citoplasmatica che rappresenta circa il 6-8% di tutta la cTnT 2 . Isoforme specifiche delle troponine cardiache I e T sono presenti esclusivamente nei miociti cardiaci, pertanto un loro incremento nel sangue testimonia inequivocabilmente un aumentato rilascio dal tessuto miocardico 3 . Le sequenze amminoacidiche delle isoforme scheletrica e cardiaca di TnT e TnI sono infatti sufficientemente diverse per poter essere differenziate utilizzando anticorpi monoclonali specifici 4,5 . A differenza di TnI e TnT, TnC non ha una isoforma cardiospecifica (il muscolo cardiaco e quello liscio codificano una proteina identica); il suo utilizzo clinico nella diagnostica cardiologica è quindi limitato dall'impossibilità di riconoscerne la fonte specifica di rilascio in circolo. Il rilascio di troponina cardiaca dal miocita al sangue può essere prodotto da un danno cellulare reversibile o irreversibile. Durante un'ischemia prolungata, le cellule sono danneggiate irreversibilmente, la membrana cellulare è degradata e sono quindi rilasciati complessi citosolici legati alle miofibrille 1 . Malgrado TnI e TnT manifestino un'efficienza diagnostica globalmente confrontabile, sono caratterizzate da una parziale eterogeneità biochimica, analitica e clinica. In seguito a una lesione miocardica, entrambe tendono ad aumentare nel plasma entro 4-12 ore, raggiungono il picco dopo 12-48 ore e ritorna-

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Factors associated with increased serum levels of cardiac troponins T and I in chronic haemodialysis patients: Chronic Haemodialysis And New Cardiac Markers Evaluation (CHANCE) study

Abstract: Elevated baseline serum levels of cardiac troponins were associated with cardiovascular risk factors, history of ischaemic heart disease and left ventricular hypertrophy in asymptomatic chronic haemodialysis patients.

Cited by 101 publications

References 18 publications

The significance of serum troponin T in patients with kidney disease: a review of the literature

The significance of serum troponin T in patients with kidney disease: a review of the literature

Predictive Value of Cardiac Troponin I and T for Subsequent Death in End-Stage Renal Disease

Cardiospecific troponins in non-ischemic cardiological pathologies

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