Home Current issue Ahead of print Search About us Editorial board Archives Submit article Instructions Subscribe Contacts Login 
  • Users Online:
  • Home
  • Print this page
  • Email this page

 Table of Contents  
Year : 2014  |  Volume : 1  |  Issue : 2  |  Page : 60-66

Prognostic Significance of Cardiac Troponin-T Level in Chronic Kidney Disease Patients on Hemodialysis

1 Department of Medicine, King George Medical University, Lucknow, Uttar Pradesh, India
2 Department of Obstetrics and Gynaecology, King George Medical University, Lucknow, Uttar Pradesh, India
3 Department of Physiology, Career Institute of Medical Sciences, Lucknow, Uttar Pradesh, India

Date of Web Publication27-Oct-2014

Correspondence Address:
Munna Lal Patel
Department of Medicine, King George Medical University, C-28, Sec-J Aliganj, Lucknow - 226 024, Uttar Pradesh
Login to access the Email id

Source of Support: None, Conflict of Interest: None

DOI: 10.4103/2225-1243.143380

Rights and Permissions

Background: Cardiovascular complications are a major cause of mortality in chronic kidney patients (CKD) patients. More than 50% of patients of end-stage renal disease (ESRD) die due to these complication. Patients undergoing chronic hemodialysis (HD) presented with frequently elevated baseline values of cardiac troponin T (cTnT). Aim of the Study: The aim of this study was to estimate the level of cTnT in ESRD patients and to evaluate its diagnostic and prognostic value in HD patients. Materials and Methods: This was a case-control study carried over a period of 14 months. One hundred and one cases of CKD stage-V as per the KDIGO guidelines 2012 with eGFR ≤15 mL/min and 50 healthy control age-matched with a GFR ≥60 mL/min were included in the study. cTnT levels were measured at the start of the study, at 48 h and 6 months after completion of hemodialysis. Results: The mean age of the controls and cases were 45.74 ± 9.99 years and 47.77 ± 17.53 years, respectively. Of 101 cases, 40 cases had cTnT levels <0.01 ng/L, 16 cases had cTnT levels 0.01-0.029 ng/mL, 20 cases had cTnT levels 0.03-0.099 ng/mL and 25 cases were had cTnT levels >0.10 ng/mL. Cardiac events were observed in 20 patients. Three patients died due to myocardial injury (cTnT levels >0.10 ng/mL) and 17 patients experienced cardiovascular events. These cardiovascular events were sudden cardiac deaths, stroke, atrial-ventricular block and congestive heart failure. Conclusion: All patients on chronic hemodialysis should be evaluated for annual measurement of serum cTnT, which could be used as a reference point. A small increase over time is common, but if any time levels more than double the baseline, which is uncommon, and if found indicate an acute coronary syndrome.

Keywords: Cardiac troponin T, cardiovascular risk factor, hemodialysis

How to cite this article:
Patel ML, Sachan R, Singh P, Chaudhary SC, Sachan P, Gupta P. Prognostic Significance of Cardiac Troponin-T Level in Chronic Kidney Disease Patients on Hemodialysis. J Integr Nephrol Androl 2014;1:60-6

How to cite this URL:
Patel ML, Sachan R, Singh P, Chaudhary SC, Sachan P, Gupta P. Prognostic Significance of Cardiac Troponin-T Level in Chronic Kidney Disease Patients on Hemodialysis. J Integr Nephrol Androl [serial online] 2014 [cited 2023 Dec 4];1:60-6. Available from: http://www.journal-ina.com/text.asp?2014/1/2/60/143380

  Introduction Top

End-stage renal disease (ESRD) patients receiving hemodialysis (HD) are at increased risk for deaths due to cardiovascular complication. In the US, approximately 4.5% of the population suffered from stage 3 and 4 chronic kidney disease (CKD). The incidence of ESRD is 330 cases per million population per year. [1],[2],[3] The approximate prevalence of CKD in India is 800 per million population, and the incidence of ESRD is 150-200 per million population. [4]

Cardiovascular complications are a major cause of mortality, and more than 50% of patients of ESRD die due to these complications. [5] According to recent studies, it was observed that recurrent episodes of myocardial ischemia and transient segmental left ventricular wall-motion abnormalities commonly occur in patients of ESRD on standard thrice-weekly HD. [6],[7],[8],[9] These repeated episodes of myocardial insult can eventually lead to scarring and irreversible loss of contractile function and are supposed to be main the pathophysiological cause of excess cardiovascular mortality in HD patients. [10]

Cardiac troponin T (cTnT) is a sensitive and specific marker of myocardial injury in the general population, which is less ascertained in patients undergoing chronic HD who have frequently elevated baseline values of cTnT. Still, controversy remains on the clinical usefulness of measuring troponins for the diagnosis of acute ischemic cardiac events in these subjects. Accumulation of immunoreactive fragments of cardiac troponins due to reduced renal clearance or continuous cardiac release from small areas of clinically silent myocardial necrosis might be responsible for elevated cTnT. [11],[12] Other possible hypotheses are the re-expression of cTnT isoforms in the skeletal muscle fibers during uremia-induced skeletal myopathy, [13] the increase in left ventricular mass index (LVMI), the loss of membrane integrity, constant outflow from the free cytosolic troponin pool and uremic damage on myocardial cells.

Therefore, to determine the degree of fluctuation in serum cTnT levels in patients that occurs both during HD and over the course of a 6-month period, we followed the patients for 11 months to determine the correlation between baseline cTnT level with patient outcome. This study was planned with the aim of estimating the level of cTnT in ESRD patients and to evaluate its diagnostic and prognostic significance in HD patients.

  Materials and Methods Top

This case-control study was carried out over a period of 14 months in the Department of Medicine in collaboration with the Department of Pathology, King George's Medical University, Lucknow, UP, India. Patients with ESRD attending the medical OPD or admitted in indoor wards for dialysis were enrolled in this study after obtaining written, informed consent. Ethical clearance from the institutional ethics committee was obtained. All the new cases of ESRD aged between 18 and 65 years who required HD were included in the study. Enrolment was performed in first 3 months and these patients were followed for 11 months. Fifty age- and gender-matched healthy controls with a GFR ≥60 mL/min and 101 cases of CKD stage-V patients with a GFR ≤15 mL/min were enrolled in this study as per the KDIGO guidelines 2012. The laboratory researcher was unaware of the baseline clinical status of the patients. Baseline clinical data and outcome of patients was recorded by the clinician who was unaware of the laboratory results. Blinding was maintained until the study was completed. The patients with known case/past history of coronary artery disease (CAD), diabetic nephropathy, acute renal failure due to any cause and malignancy, and those subjects who were not willing to take part in the study were excluded from the study.

Cerebrovascular disease was established if patients had a history of transient ischemic attack or stroke confirmed by computed tomography. Cardiovascular events were defined as myocardial ischemia/injury, sudden cardiac deaths, atrial-ventricular block and congestive heart failure. Hypertension was diagnosed as blood pressure of 140/90 mmHg or greater. Left ventricular hypertrophy was defined by ECG as R-wave amplitude ≥25 mm deflection in any precordial leads, R-wave amplitude ≥20 mm in standard leads, R-wave amplitude ≥11 mm in augmented unipolar leads, R-wave amplitude in V5 or V6 plus S-wave amplitude in V1 or V2 ≥35 mm, ST segment characteristically depressed and flattened to inverted T wave. [14],[15]

Both case and control recruited in the study underwent biochemical examination. Ten milliliters of venous blood sample was withdrawn with full aseptic precaution after an overnight fast. About 8 mL of blood was collected directly into sterilized vacuum tubes containing no additives and 2 mL of blood was separated in an EDTA vial. The blood was centrifuged at 5000 rpm for 10 min at room temperature and serum was separated and stored at -70 0 C until complete biochemical analysis was performed. Routine biochemical variables were measured using standardized method on autoanalyzers. CTnT was measured by electrochemiluminescence immunoassay (ECLIA) on Elecsys and cobas-e immunoassay analyzers-Roche Diagnostics, (Patent No. US 6376206 an US 6333397) Mannheim, Germany . This assay detects up to 0.01 ng/L, and values above this gives a quantitative reading. Our laboratory reference range for minimal myocardial necrosis and myocardial infarction was 0.03-0.1 and >0.1 mg/L, respectively. Pre-dialysis and post-dialysis serum cTnT levels were measured 30 min before dialysis, at 48 h and 6 months. The cases were subjected to HD on a B-brown machine using a polysulfone dialyser (1.5 m 2 ) for 4 h every alternate day.

The end point of the study was fatal or non-fatal cardiovascular events. Outcome was recorded by a nephrologist who was unaware of the cTnT level until the final study. All cardiovascular events were verified by a clinician not involved in the study. Patients who were enrolled for HD therapy were explained regarding cardiovascular events like sudden cardiac death and acute myocardial infarction as per the Consensus Document of the Joint European Society of Cardiology/American College of Cardiology Committee for redefinition of myocardial infarction. [16]

Statistical analysis

Data were summarized as mean ΁ SD. Groups were compared by the Independent Student's test. Groups were also compared by one-way analysis of variance (ANOVA) and the significance of mean difference between the groups was analyzed by the Tukey's post hoc test. Paired groups were compared by the paired t test. Discrete (categorical) groups were compared by the chi-square (χ2 ) test. Hazard ratios were calculated using the Cox regression analysis. Survival between the two groups was compared by the Kaplan-Meier method using the Log rank test. The diagnostic accuracy of cTnT was analyzed by using the (receiver operating characteristic (ROC) curve analysis. A two-sided (α = 2) P < 0.05 was considered statistically significant. All analyses were performed on STATISTICA software (Windows version 6.0).

  Results Top

The mean (΁SD) age of the controls and cases was 45.74 ΁ 9.99 years and 47.77 ΁ 17.53 years, respectively. Further, in controls, there were 25 males (50.0%) and 25 females (50.0%) while in the cases, 34 (33.7%) were male and 67 (66.3%) were female. In our study, among 101 cases, 42.6% were hypertensive, 17.8% had ECG changes and 37.6% were on antihypertensive medication. The maximum number of patients were of chronic glomerulonephritis (47.5%), followed by hypertensive nephropathy (42.6%), obstructive nephropathy (4.0%), adult polycystic kidney disease (ADPKD) (3.0%) and nephrotic syndrome (2.0%) [Table 1].

A statistically significant association of cTnT was observed with respect to traditional cardiovascular risk factors such as age >40 years, male gender, hypertension, diabetes, ECG changes and history of smoking (P < 0.05). This indicates that cases were relatively at higher risk for cardiovascular events as compared with controls [Table 2].

In univariate Cox regression analysis, patients with detectable cTnT levels had cardiovascular risk 12.45-times (95% CI, 4.91-31.02; P < 0.000) greater than those with undetectable cTnT levels. Patients with CKD who were aged >40 years had cardiovascular risk increases 1.11 times per year (P < 0.0017). If they have left ventricular hypertrophy LVH, then cardiovascular risk increases 5.25 times (P < 0.0003). Patient who had a decrease in eGFR (P < 0.0012) and anemia were at higher risk for cardiovascular events [Table 3].

cTnT levels were undetectable in almost all controls, except two subjects (cTnT < 0.01 ng/mL), and levels were increased in the cases. Of 101 cases, 40 cases had cTnT levels < 0.01 ng/L, 16 cases had cTnT levels 0.01-0.029 ng/mL, 20 cases had cTnT levels 0.03-0.099 ng/mL and 25 cases had cTnT levels >0.10 ng/mL. Of the 101 patients with increased cTnT level, cadiac events developed in 20 patients [Table 4]. Three patients died during the follow-up period due to myocardial injury (cTnT levels >0.10 ng/mL). The other 17 patients experienced cardiovascular events such as sudden cardiac deaths, atrial-ventricular block, thrombosis and congestive heart failure during the follow-up period of 11 months [Table 5].

When we observed survival distribution with different levels of troponin, Trop-T levels >0.1 had minimum survival. To determine the effect of cTnT on survival, Trop T was subgrouped into two groups according to the respective median cut-off values. The Kaplan-Meier Log rank test showed significantly different and lower survivals in patients who had cTnT >0.03 ng/mL on admission as compared with those having cTnT ≤0.03 ng/mL (χ2 = 31.52, DF = 1; P < 0.001) [Figure 1] and [Figure 2].

Diagnostic accuracy (cut-off or criterion value) of cTnT was evaluated. The marker levels on admission were further analyzed with final outcome (death and live) using ROC curve analysis [Figure 3]. The cTnT at cut-off value ≥0.095 ng/mL showed the highest sensitivity of 100% (95% CI = 95.0-100.0) with high specificity of 96.55% (95% CI = 82.2-99.4), with a positive predictive value of 98.6% and a negative predictive value of 100.0% [Table 6].

  Discussion Top

Patients with renal disease, especially those undergoing HD therapy, are likely to have CAD. Cardiovascular disease is the leading cause of death in ESRD populations, and represents approximately 50% of all deaths. [17],[18] In nonuremic patients with suspected myocardial damage, determination of myoglobin, creatine kinase-MB (CK-MB) and troponin levels have proved reliable for early diagnosis. [19],[20] However, high serum concentrations of myoglobin and CK-MB lack specificity and thus elevated baseline serum levels of cardiac troponin have been reported more specifically in HD patients. [21],[22],[23]

It is unclear how elevated troponin levels should be interpreted in patients with CKD and which factors could influence these determinants. It remains uncertain whether the threshold values account for false-positive diagnosis of minimal myocardial damage and whether cardiac troponins are of prognostic value in patients with moderate CKD. However, data are scarce in clinically stable HD patients. Increased cTnT levels in clinically stable HD patients represent a strong and independent predictor of cardiovascular mortality. More recently, three large observational studies found that the cTnT level is associated strongly with the risk of cardiovascular events in HD patients. [24],[25]

Measurement of serum cTnT has revolutionized the management of acute coronary syndrome. [26],[27] However, increased serum cardiac troponin levels are observed frequently in patients with CKD, even when suspicion of active ischemia is relatively low. However, in HD patients, the prevalence of elevated cTnT levels is greater. It is unknown whether uremia can alter the detection, release or clearance of different troponin subunits in serum. It is likely that elevated serum troponin levels are the result of decreased clearance by the diseased kidney because free and bound cTnT are relatively large molecules.

Therefore, it is possible that the greater cTnT level in patients with CKD may reflect reduced GFR. However, 40 patients with CKD in our study had undetectable/insignificant increased cTnT levels. Arteriosclerotic effects, nonarteriosclerotic effects (concentric and eccentric LVH, volume overload, myocardial fibrosis, decreased arterial compliance and intima-media thickness) may lead to a decrease in myocardial blood flow, causing minimal ischemic lesions. This can produce the release of small amounts of intracellular proteins, such as troponin, into the blood of hemodialyzed patients. [28],[29]

In our study, we found that the cTnT concentration was <0.01 ng/mL in 40 patients (39.6%), <0.03 ng/mL in 16 patients (15.8%), 0.03-0.099 ng/mL in 20 patients (19.8%) and >0.1 ng/mL in 25 patients (24.75%). Increase in the level of cTnT demonstrates the potential validity of increased serum cTnT level in subjects before HD in the absence of an acute coronary event [Table 4]. In the presence of an acute coronary syndrome, however, serum cTnT levels were substantially increased as compared with baseline, although a small increase occurred in the majority of patients. This small increase may reflect coronary atherosclerosis or LVH or a reduction in residual renal function with cumulative time spent on dialysis.

Our study suggested that intradialytic rise in cTnT may occur as a result of hemoconcentration due to ultrafiltration. However, it is possible that they may reflect coronary insufficiency induced by hypotension during dialysis in patients with fixed coronary artery stenosis. It has been hypothesized that HD patients may have elevated cTnT levels because of volume overload, causing myocardial stretch and cTnT leakage. In a recent study, the author suggested that cTnT is independently linked to left ventricular mass in clinically stable dialysis patients.The relationship between LVH and myocardial ischemia is well established. However, a recent study reported that the prevalence of LVH was not different based on high or low cTnT values. In this study, LVH was diagnosed by echocardiography and the majority of patients presented with LVH. [30]

In our study, age, gender, diabetes, hypertension, LVH, anemia and smoking had a positive correlation with cardiac troponin with slight elevations in cTnT levels. All these factors were responsible for an increase in cardiovascular risk in patients with CKD. These results are similar to works performed by others in HD patients. [31],[32] It has been hypothesized that HD patients may have elevated cTnT levels because of volume overload, causing myocardial stretch and cTnT leakage. [33]

In our study, the greater prevalence of previous CHF episodes was found to be the main factor for increasing cTnT levels thus indicating that chronic heart failure can elevate cTnT levels. Release of cardiac troponin in chronic heart failure may result from apoptotic cell death in ventricular remodeling. [34] Recently, it was shown that cTnT is independently linked to left ventricular mass in clinically stable dialysis patients. The relationship between LVH and myocardial ischemia is well established and based on several mechanisms. However, a recent work showed that all patients with increased cTnT levels had significant cardiac histological changes. [35] Furthermore, increased cTnT levels, even in the absence of acute ischemia, are indicative of compromised myocardium.

The ROC curve depicted that, after adjustment for other risk factors, the cut-off value for myocardial infarction detection was ≥0.095 ng/mL with sensitivity of 100.00% (95.0-100.0) and specificity of 96.55% (82.2-99.4) at the 95% confidence interval. The positive predictive value was 100.0. Our finding is compatible to the study done by another author who reported cTnT above 0.1 ng/mL as the cut-off value (HR 2.2; 95% CI, 1.1-4.4; P = 0.02). [36]

In this study, overall survival in cases according to the Trop T level showed significantly different and lower survival in patients who had rop T >0.03 ng/mL on admission as compared with those who had Trop T levels <0.03 ng/mL (x 2 = 31.52; P < 0.001). A study performed by another author in chronic HD patients reported that elevated baseline cTnT levels were associated with an increased risk of mortality or ACS at 18 months (P = 0.0015). [37] Another study in CKD subjects reported that after a mean follow-up of 12.9 months, about 17% mortality occurred due to cardiovascular events. [38]

The cTnT cut-off value used to evaluate mortality and cardiovascular risk deferred in different studies. Two studies and a recent metaanalysis [39] suggested that a cTnT concentration >0.1 ng/L identified in a subgroup of asymptomatic ESRD patients had poor survival rate and high risk of cardiac death. There is increasing evidence that an even lower cTnT cut-off value <0.1 ng/L was predictive of increased cardiovascular mortality. [40],[41]

Our study was supported by others in terms of patient survival and patient with an elevation of baseline cTnT concentration >0.03 μg/L, the risk of death due to acute coronary syndrome was significantly greater (P = 0.0015) and the degree of risk was dependent on the magnitude of the elevation in baseline cTnT. Cardiovascular complications represent a fundamental factor limiting survival in patients with advanced renal disease. Therefore, it is important to identify and validate a new simple marker that reflects the risk associated with cardiac ischemia. Elevated cTnT levels predict adverse outcomes in patients with cardiac ischemia. In the past years, few studies have shown that cTnT levels predict cardiovascular complications and mortality in HD patients. [42]

All patients on chronic hemodialysis should have an annual measurement of serum cTnT, levels that could be used as a reference point. A small increase over time is common, but levels more than double the baseline are alarming and may indicate an ACS. This could be confirmed by dynamic cTnT changes on subsequent measurements, dependent on the timing of sampling with respect to the onset of chest pain.

Limitations of our study

Because of limited resources, we do not have echocardiographic or angiographic information of the patients. A diagnosis of myocardial infarction/angina was based on the clinical evaluation by the treating physician and the cause of death was not determined by postmortem examination. It is possible that some of the sudden cardiac deaths were due to hyperkalemia rather than an acute coronary syndrome.

  References Top

US Renal Data System: USRDS 2005. Annual Data Report: Atlas of End stage renal disease in the United States, Bethesda, MD: National Institute of Health, National Institute of Diabetes and Digestive and Kidney Diseases; 2005.  Back to cited text no. 1
Jones CA, McQuillan GM, Kusek JW, Eberhardt MS, Herman WH, Coresh J, et al. Serum creatinine levels in the US population: Third National Health and Nutritional Examination Survey. Am J Kidney Dis 1998;32:992-9.  Back to cited text no. 2
Coresh J, Astor BC, Greene T, Eknoyan G, Levey AS. Prevalence of chronic kidney disease and decreased kidney function in the adult US population. 3 rd National health and Nutrition Examination Survey. Am J Kidney Dis 2003;41:1-12.  Back to cited text no. 3
Agarwal SK, Srivastava RK. Chronic Kidney Disease in India: Challenges and Solutions. Nephron Clin Pract 2009;111:c197-203.  Back to cited text no. 4
National Institutes of Health: USRDS 2008 Annual Data Report. Bethesda, MD, US Renal Data System, 2008.  Back to cited text no. 5
McIntyre CW, Burton JO, Selby NM, Leccisotti L, Korsheed S, Baker CS, et al. Hemodialysis-induced cardiac dysfunction is associated with an acute reduction in global and segmental myocardial blood flow. Clin J Am Soc Nephrol 23008;3:19-26.  Back to cited text no. 6
Burton JO, Jefferies HJ, Selby NM, McIntyre CW. Hemodialysis induced cardiac injury: Determinants and associated outcomes. Clin J Am Soc Nephrol 2009;4:914-20.  Back to cited text no. 7
Dasselaar JJ, Slart RH, Knip M, Pruim J, Tio RA, McIntyre CW, et al. Haemodialysis is associated with a pronounced fall in myocardial perfusion. Nephrol Dial Transplant 2009;24:604-10.  Back to cited text no. 8
Breidthardt T, McIntyre CW. Dialysis-induced myocardial stunning: The other side of the cardiorenal syndrome. Rev Cardiovasc Med 2011;12:13-20.  Back to cited text no. 9
Braunwald E, Kloner RA. The stunned myocardium: Prolonged, postischemic ventricular dysfunction. Circulation 1982;66:1146-9.  Back to cited text no. 10
Mallamaci F, Zocalli C, Parlongo S, Tripepi G, Benedetto FA, Cutrupi S, et al. Troponin is related to left ventricular mass and predicts all-cause cardiovascular mortality in haemodialysis patients. Am J Kidney Dis 2002;40:68-75.  Back to cited text no. 11
Diris JH, Hackeng CM, Kooman JP, Pinto YM, Hermens WT, van Dieijen-Visser MP. Impaired renal clearance explains elevated troponin T fragments in hemodialysis patients. Circulation 2004;109:23-5.  Back to cited text no. 12
Freda BJ, Tang WH, Van Lente F, Peacock WF, Francis GS. Cardiac troponin in renal insufficiency: Review and clinical implications. J Amer Coll Cardiol 2002;40:2065-71.  Back to cited text no. 13
Weiner DE, Tighiouart H, Vlagopoulos PT, Griffith JL, Salem DN, Levey AS, et al. Effect of anaemia & left ventricular hypertrophy on cardiovascular disease in patient with chronic kidney disease. J Am Soc Nephrol 2005;16:241-7.  Back to cited text no. 14
Kannel WB, Feinleib M, McNamara PM, Garrison RJ, Castelli WP. An investigation of coronary heart disease in families. The F framingham offspring study. Am J Epidemiol 1979;110:281-90.  Back to cited text no. 15
Alpert JS, Thygessen K, Antman E, Bassaand JP. Myocardial infarction redefined-A consensus document of the Joint European Society of Cardiology/American College of Cardiology Committee for the redefinition of myocardial infarction. J Am Coll Cardiol 2000;36:959-69.  Back to cited text no. 16
Culleton BF, Larson MG, Wilson PW, Evans JC, Parfrey PS, Levy D. Cardiovascular disease and mortality in a community-based cohort with mild renal insufficiency. Kidney Int 1999;56:2214-9.  Back to cited text no. 17
Foley RN, Parfrey PS, Sarnak MJ. Clinical epidemiology of cardiovascular disease in chronic renal failure. Am J Kidney Dis 1998;32(5 suppl 3):S112-9.  Back to cited text no. 18
Panteghini M, Pagani F, Bonetti G. The sensitivity of cardiac markers: An evidence-based approach. Clin Chem Lab Med 1999;37:1097-106.  Back to cited text no. 19
Chapelle JP. Cardiac troponin I and troponin T: Recent players in the field of myocardial markers. Clin Chem Lab Med 1999;37:11-20.  Back to cited text no. 20
Iliou MC, Fumeron C, Benoit MO, Tuppin P, Courvoisier CL, Calonge VM, et al. 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. Nephrol Dial Transplant 2001;16:1452-8.  Back to cited text no. 21
Lang K, Schindler S, Forberger C, Stein G, Figulla HR. Cardiac troponins have no prognostic value for acute and chronic cardiac events in asymptomatic patients with end-stage renal failure. Clin Nephrol 2001;56:44-51.  Back to cited text no. 22
George SK, Singh AK. Current markers of myocardial ischemia and their validity in end-stage renal disease. Curr Opin Nephrol Hypertens 1999;8:719-22.  Back to cited text no. 23
Ooi DS, Zimmerman D, Graham J, Wells GA. Cardiac troponin T predicts long-term outcomes in hemodialysis patients. Clin Chem 2001;47:412-7.  Back to cited text no. 24
Dierkes K, Domrose U, Westphal S, Ambrosch A, Bosselmann HP, Neumann KH, et al. Cardiac troponin T predicts mortality in patients with end-stage renal disease. Circulation 2000;102:1964-9.  Back to cited text no. 25
Herzog CA, Apple FS. Cardiac biomarkers in the new millennium. Semin Dial 2001;14:322-3.  Back to cited text no. 26
Filatov VL, Katrukha AG, Bulargina TV, Gusev NB. Troponin: Structure, properties, and mechanism of functioning. Biochemistry (Mosc) 1999;64:969-85.  Back to cited text no. 27
London GM, Parfrey PS. Cardiac disease in chronic uremia pathogenesis. Adv Ren Replace Ther 1997;4:194-211.  Back to cited text no. 28
Frankel WL, Herold DA, Ziegler TW, Fitzgerald RL. Cardiac troponin T is elevated in asymptomatic patients with chronic renal failure. Am J Clin Pathol. 1996;106:118-23.  Back to cited text no. 29
deFilippi C, Wasserman S, Rosanio S, Tiblier E, Sperger H, Tocchi M, et al. Cardiac troponin T and C-reactive protein for predicting prognosis, coronary atherosclerosis, and cardiomyopathy in patients undergoing long-term hemodialysis. JAMA 2003;290:353-9.  Back to cited text no. 30
Ooi DS, House AA. Cardiac troponin T in hemodialysed patients. Clin Chem 1998;44:1410-6  Back to cited text no. 31
Aviles RJ, Askari AT, Lindahl B, Wallentin L, Jia G, Ohman EM, et al. Troponin T levels in patients with acute coronary syndromes, with or without renal dysfunction. N Engl J Med 2002;346:2047-52.  Back to cited text no. 32
Wang AY, Lai KN. Use of Cardiac Biomarkers in End-Stage Renal Disease. J Am Soc Nephrol 2008;19:1643-52.  Back to cited text no. 33
Setsusa K, Ohtsuka T, Ogawa T. Prognostic value of second generation cardiac troponin T in patients with chronic heart failure. J Am Coll Cardiol 1998;31:S249.  Back to cited text no. 34
Ooi D, Isotalo PA, Veinot JP. Correlation of antemortem serum creatine kinase, creatine kinase-MB, troponin I, and troponin T with cardiac pathology. Clin Chem 2000;46:338-44.  Back to cited text no. 35
Kalaji FR, Albitar S. Predictive value of Cardiac Troponin T and I in Hemodialysis patients. Saudi J Kidney Dis Transpl 2012;23:939-45.  Back to cited text no. 36
[PUBMED]  Medknow Journal  
Conway B, McLaughlin M, Sharpe P, Harty J. Use of cardiac troponin T in diagnosis and prognosis of cardiac events in patients on chronic haemodialysis. Nephrol Dial Transplant 2005:20;2759-64.  Back to cited text no. 37
Goicoechea M, Garcýéa de Vinuesa S, Gómez-Campderá F, Gutierrez MJ, Blanco P, Amann R, et al. Clinical significance of cardiac troponin T levels in chronic kidney disease patients: Predictive value for cardiovascular risk. Am J Kidney Dis 2004;43:846-53.  Back to cited text no. 38
Khan NA, Hemmelgarn BR, Tonelli M, Thompson CR, Levin A. Prognostic value of troponin T and I among asymptomatic patients with end-stage renal disease: A meta-analysis. Circulation 2005;112:3088-96.  Back to cited text no. 39
Duman D, Tokay S, Toprak A, Duman D, Oktay A, Ozener IC, et al. Elevated cardiac troponin T is associated with increased left ventricular mass index and predicts mortality in continuous ambulatory peritoneal dialysis patients. Nephrol Dial Transplant 2005;20:962-7.  Back to cited text no. 40
Havekes B, van Manen JG, Krediet RT, Boeschoten EW, Vanderbroucke JP, Dekker FW; for the NECOSAD Study Group. Serum troponin T concentration as a predictor of mortality in hemodialysis and peritoneal dialysis patients. Am J Kidney Dis 2006;47:823-9.  Back to cited text no. 41
Apple FS, Murakami MM, Pearce LA, Herzog CA. Predictive value of cardiac troponin I and T for subsequent death in end-stage renal disease. Circulation 2002;106:2941-5.  Back to cited text no. 42


  [Figure 1], [Figure 2], [Figure 3]

  [Table 1], [Table 2], [Table 3], [Table 4], [Table 5], [Table 6]


Similar in PUBMED
   Search Pubmed for
   Search in Google Scholar for
 Related articles
Access Statistics
Email Alert *
Add to My List *
* Registration required (free)

  In this article
Materials and Me...
Article Figures
Article Tables

 Article Access Statistics
    PDF Downloaded738    
    Comments [Add]    

Recommend this journal