Cardiac troponin I (2nd generation assay) in chronic haemodialysis patients: prevalence and prognostic value

M, Beciani; Tedesco, Angela; Violante, Anneo; Cipriani, Silvia; Azzarito, Michele; Sturniolo, A.; Splendiani, G

doi:10.1093/ndt/gfg057

Cited by 39 publications

(42 citation statements)

References 18 publications

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“…(8 -12 )]. Most studies have focused on hemodialysis patients, in whom increased cardiac troponin concentrations are associated with increasing age, presence of cardiovascular risk factors, history of ischemic heart disease, diabetes, and LVH (13)(14)(15) and predict increased cardiac and all-cause mortality (15)(16)(17)(18)(19)(20)(21).…”

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confidence: 99%

Cardiac Troponins and Renal Function in Nondialysis Patients with Chronic Kidney Disease

et al. 2005

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Background: Serum cardiac troponin concentrations are commonly increased in end-stage renal disease (ESRD) in the absence of an acute coronary syndrome (ACS). The data on cardiac troponin I (cTnI) are more variable than those for cardiac troponin T (cTnT). There is little information on cardiac troponin concentrations in patients with chronic kidney disease (CKD) who have not commenced dialysis. Methods: We studied 222 patients: 56 had stage 3 (moderate CKD); 70 stage 4 (severe CKD); and 96 stage 5 (kidney failure). Patients underwent echocardiography and were followed prospectively for a median of 19 months; all-cause mortality was recorded. Results: Overall, serum cTnT was increased above the 99th percentile reference limit in 43% of all CKD patients studied, compared with 18% for cTnI. Serum cTnT and cTnI concentrations were more commonly increased in the presence of more severe CKD (11 and 6 patients in stage 3, 27 and 8 in stage 4, and 57 and 24 in stage 5 (P <0.0001 and <0.02, respectively). Among 38 patients with detectable cTnI, 32 had detectable cTnT (r s ‫؍‬ 0.67; P<0.0001). There was evidence that decreasing estimated glomerular filtration rate increased the odds of having detectable cTnT (P <0.001) but not cTnI (P ‫؍‬ 0.128). There was no evidence to support an adjusted association of detectable cardiac troponins with increasing left ventricular mass index. Increased cTnT (P ‫؍‬ 0.0097), but not cTnI, was associated with decreased survival. Conclusions: Increased cTnT and cTnI concentrations are relatively common in predialysis CKD patients, in

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confidence: 99%

Cardiac Troponins and Renal Function in Nondialysis Patients with Chronic Kidney Disease

et al. 2005

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“…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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“…13 The relationship between cTnI and mortality is more controversial than that between mortality and cTnT. [4][5][6][12][13][14][15] A majority of these studies demonstrated that elevated cTnI is not an independent predictor for death; 4,6,12,13,15 again, these studies did not determine LVH and/or LVMI.…”

Section: Prognostic Utility Of Troponins In End-stage Renal Diseasementioning

confidence: 99%

“…10,11 Several previous studies have also evaluated the prognostic utility of troponins in patients with ESRD. [3][4][5][6][12][13][14][15] The majority of these studies demonstrated that troponin elevation is a strong, independent prognostic indicator for short-and longterm adverse outcomes. 3-5, 14, 15 However, other studies failed to confirm the association between troponin and death in patients with ESRD.…”

Section: Introductionmentioning

confidence: 99%

Cardiac troponins T and I in patients with end‐stage renal disease: The relation with left ventricular mass and their prognostic value

Abacı

Ekıcı

Oğuzhan

et al. 2004

Clinical Cardiology

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SummaryBackground: Cardiac troponins are frequently elevated in patients with end-stage renal disease (ESRD) in the absence of acute myocardial ischemia. The cause and prognostic value of cardiac troponin elevations in such patients are controversial.Hypothesis: The aims of this study were (1) to define the incidence of cTnT and cTnI elevations in patients with ESRD, (2) to evaluate the relationship between troponin elevations and left ventricular mass index (LVMI), and (3) to evaluate the prognostic value of elevations in cTnT and cTnI prospectively.Methods: We included 129 patients with ESRD (71 men, age 44 ± 16 years) with no clinical evidence of coronary artery disease. All patients underwent cardiac examinations, including medical history, physical examination, electrocardiogram, and transthoracic echocardiography. Left ventricular mass index was calculated and all patients were followed for 2 years.Results: The cTnT concentration was > 0.03-0.1 ng/ml in 27 (20.9%) and > 0.1 ng/ml in 27 (20.9%) of the 129 patients. The cTnI concentration was > 0.5 ng/ml in 31 (24%) of 129 patients. Multiple logistic regression analysis identified LVMI (p < 0.001), diabetes (p = 0.001), and serum albumin level (p = 0.009) as a significant independent predictor for elevated cTnT. Left ventricular mass index was the only significant independent predictor for elevated cTnI (p = 0.002). There were

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Cardiac troponin I (2nd generation assay) in chronic haemodialysis patients: prevalence and prognostic value

Cited by 39 publications

References 18 publications

Cardiac Troponins and Renal Function in Nondialysis Patients with Chronic Kidney Disease

Cardiac Troponins and Renal Function in Nondialysis Patients with Chronic Kidney Disease

Cardiospecific troponins in non-ischemic cardiological pathologies

Cardiac troponins T and I in patients with end‐stage renal disease: The relation with left ventricular mass and their prognostic value

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