Skip Navigation


NDT Advance Access originally published online on December 8, 2007
Nephrology Dialysis Transplantation 2008 23(3):1019-1025; doi:10.1093/ndt/gfm738
This Article
Right arrow Abstract Freely available
Right arrow FREE Full Text (PDF) Freely available
Right arrow All Versions of this Article:
23/3/1019    most recent
gfm738v1
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Services
Right arrow Email this article to a friend
Right arrow Similar articles in this journal
Right arrow Similar articles in ISI Web of Science
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Add to My Personal Archive
Right arrow Download to citation manager
Right arrow Search for citing articles in:
ISI Web of Science (3)
Right arrowRequest Permissions
Right arrow Disclaimer
Google Scholar
Right arrow Articles by Connolly, G. M.
Right arrow Articles by Maxwell, A. P.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Connolly, G. M.
Right arrow Articles by Maxwell, A. P.
Social Bookmarking
Add to CiteULike   Add to Connotea   Add to Del.icio.us  
What's this?

© The Author [2007]. Published by Oxford University Press on behalf of ERA-EDTA. All rights reserved. For Permissions, please e-mail: journals.permissions@oxfordjournals.org


Troponin T is an independent predictor of mortality in renal transplant recipients

Grainne M. Connolly1, Ronan Cunningham2, Peter T. McNamee2, Ian S. Young1 and Alexander P. Maxwell2

1 Department of Clinical Biochemistry, Royal Victoria Hospital 2 Department of Nephrology, Belfast City Hospital, Belfast, Northern Ireland BT12 6BA, UK

Dr Grainne Connolly, Department of Clinical Biochemistry, Royal Victoria Hospital, Grosvenor Road, Belfast, Northern Ireland BT12 6BA, UK. Tel: +44-2890240503; Fax: +44-2890234029; E-mail: Grainne.Connolly{at}bll.n-i.nhs.uk



   Abstract
Top
 Abstract
Introduction
 Subjects and methods
 Biochemical analyses
 Prospective data collection
 Statistical analyses
 Results
 Discussion
 References
 
Background. Numerous reports have demonstrated an association between elevated Troponin T levels and adverse cardiovascular outcomes in patients with chronic kidney disease. However, whether raised Troponin T levels are an independent predictor of mortality in renal transplant recipients has not yet been established. The aim of this study was, therefore, to assess the use of Troponin T as a prognostic marker in a population of renal transplant recipients.

Methods. Three hundred and seventy-two asymptomatic renal transplant recipients were recruited between June 2000 and December 2002. Troponin T was measured at baseline and prospective follow-up data were collected at a median of 1739 days.

Results. In Kaplan-Meier analysis a Troponin T level ≥0.03 µg/l was a significant predictor of mortality (P < 0.001). In Cox Regression analysis, an elevated Troponin T level remained a significant predictor of mortality following adjustment for traditional cardiovascular risk factors (P < 0.001) and following adjustment for estimated glomerular filtration rate and high sensitivity C reactive protein (P < 0.001).

Conclusions. Elevated Troponin T level is a strong independent predictor of all cause mortality in patients with a renal transplant. Troponin T, therefore, represents a promising biochemical marker that identifies those renal transplant recipients who are most likely to benefit from aggressive cardiovascular risk factor modification.

Keywords: cardiovascular disease; cardiovascular events; renal transplantation; risk factors; survival



   Introduction
Top
 Abstract
 Introduction
Subjects and methods
 Biochemical analyses
 Prospective data collection
 Statistical analyses
 Results
 Discussion
 References
 
Troponin T is a key biochemical marker used in the diagnosis, prognosis and risk stratification of patients with chest pain and acute coronary syndromes. However, Troponin T levels are often elevated in asymptomatic patients with chronic renal failure [1] and raised Troponin T concentrations in such patients are an independent predictor of mortality [2]. Raised Troponin T levels in patients on haemodialysis have also been associated with other cardiovascular risk factors [3] and diffuse coronary artery disease [4]. A raised Troponin T concentration is reported to be a significant predictor of mortality in dialysis patients [4–7].

The association between Troponin T and mortality in chronic renal failure and dialysis patients is mainly due to a link between elevated Troponin T levels and adverse cardiovascular outcomes in patients with renal failure [5–11]. However, whether raised Troponin T levels are an independent predictor of mortality in renal transplant recipients has not yet been established.

The aim of this study was, therefore, to assess the use of Troponin T as a prognostic marker for mortality in a population of renal transplant recipients.



   Subjects and methods
Top
 Abstract
 Introduction
 Subjects and methods
Biochemical analyses
 Prospective data collection
 Statistical analyses
 Results
 Discussion
 References
 
Subjects
Three hundred and seventy-two renal transplant recipients were recruited consecutively from the renal transplant clinics at Belfast City Hospital and Antrim Area Hospital in Northern Ireland between June 2000 and December 2002. Ethical permission was obtained from the Research Ethics Committee, Queen's University Belfast and fully informed consent was obtained from each participant prior to enrolment. Patients were eligible for entry if they had a functioning renal transplant present for at least 3 months and although no formal exclusion criteria were imposed, patients who had chest pain or signs of sepsis at initial assessment were deferred until subsequent re-assessment.

The 372 renal transplant recipients enrolled in this study represented 70.5% of patients with a functioning renal transplant in Northern Ireland at the end of 2002. The remaining 29.5% of patients with a functioning renal transplant not enrolled in this study represent patients who did not consent to participate in the study or patients who attended transplant clinics at other hospitals in the Northern Ireland region.

For each participant, a fasting blood sample was obtained and stored at –70°C until biochemical analysis. At enrolment, patients completed a cardiovascular risk assessment questionnaire with the assistance of a research nurse. This recorded the presence of traditional cardiovascular risk factors (age, gender, diabetes and smoking), immunosuppression regimen and previous history of cardiovascular disease. A history of coronary heart disease was defined by a positive exercise stress test, coronary angiography or clinical history of angina, acute coronary syndrome or myocardial infarction, a history of peripheral vascular disease was defined by prior amputation, femoral angiogram confirmation or clinical evidence of peripheral vascular disease and a history of cerebrovascular disease was defined by a history of a cerebrovascular accident or transient ischaemic attack.

Each patient also had a measurement of weight and height (recorded using electronic scales Seca 766, and a Seca 220 measuring rod, Seca, Birmingham, UK). Blood pressure was the average of the last three blood pressure measurements (measured using Disytest sphygmomanometer Welch-Allyn, Buckinghamshire, UK) recorded at the renal transplant clinic.



   Biochemical analyses
Top
 Abstract
 Introduction
 Subjects and methods
 Biochemical analyses
Prospective data collection
 Statistical analyses
 Results
 Discussion
 References
 
Troponin T was measured to two decimal places using the Elecys Systems 1010 third generation sandwich immunoassay (Roche Diagnostics Gmbh, Mannheim, Germany). Fifteen microlitres of sample, a biotinylated monoclonal Troponin T-specific antibody and a monoclonal Troponin T-specific antibody labelled with a ruthenium complex were incubated to form a sandwich complex. Streptavidin-coated microparticles were then added and the reaction mixture was aspirated into a measuring cell, where the microparticles were magnetically captured onto the surface of the electrode. Unbound substances were removed with ProCell. Application of a voltage to the electrode induced a chemiluminescent emission which was measured by a photomultiplier and results were determined via a calibration curve. The 99th percentile value from the reference population of 1951 subjects used by the manufacturer of the assay was <0.01 µg/l and the lowest level at which the coefficient of variation was <10% was 0.03 µg/l.

Total cholesterol and high density lipoprotein cholesterol were measured using VITROS slides and analysed using a VITROS 700 System (Ortho Clinical Diagnostics, Rochester, NY, USA).

Serum creatinine was measured using the VITROS Slide System and the VITROS 950 analyser system (Ortho Clinical Diagnostics, Rochester, NY, USA). Estimated GFR (glomerular filtration rate) was calculated for all patients using a simplified 4-variable MDRD equation:


Formula

Twenty-four hour urinary protein was measured using a dye-binding technique, Microprotein PR (Sigma, Poole, UK), on a Roche Cobas Fara analyser (Roche, Basel, Switzerland). Results for 24 h urinary protein collections were available for 355 patients; the remainder of patients did not collect 24 urinary collections.

High sensitivity C reactive protein was measured using a high sensitivity immunoturbidimetric assay (Randox, Crumlin, UK). Samples were analysed using a Roche Cobas Fara (Roche, Basel, Switzerland).

Ciclosporin level was measured for all participants prescribed ciclosporin.



   Prospective data collection
Top
 Abstract
 Introduction
 Subjects and methods
 Biochemical analyses
 Prospective data collection
Statistical analyses
 Results
 Discussion
 References
 
The collection of prospective follow-up data was completed in June 2006, at a mean of 1626 days and a median of 1739 days after enrolment. Mortality data, including date of death, where applicable, was available for all participants. This information was obtained from the mortality data recorded on the Regional Nephrology Database at Belfast City Hospital and via letter and telephone contact with the Primary Care Physicians of patients enrolled in this study.



   Statistical analyses
Top
 Abstract
 Introduction
 Subjects and methods
 Biochemical analyses
 Prospective data collection
 Statistical analyses
Results
 Discussion
 References
 
Data analysis was performed using SPSS (version 12.0). For some parameters such as Troponin T, it was clear that the distribution deviated significantly from normality. For other parameters, Kolmogorov–Smirnoff analysis was used to test if variables were normally distributed.

Logarithmic transformation was performed for variables that did not conform to a normal distribution. For those variables which did not conform to a normal distribution following logarithmic transformation, analysis was performed using non-parametric tests. For normally distributed variables data are expressed as arithmetic mean ± standard deviation. For those variables that were not normally distributed data are expressed as median and interquartile range in brackets.

Correlations between continuous variables were assessed using Spearman's correlation coefficients. A two-tailed P-value <0.05 was considered to be statistically significant. Kaplan-Meier analysis with log rank test was used for univariate survival analysis. Given the size of the study population, cardiovascular risk factors (i.e. age, gender, smoking, diabetes, systolic blood pressure, total cholesterol, high density lipoprotein cholesterol and body mass index) were banded into thirds and included in a Cox Regression model for cumulative survival analysis. However since Troponin T has an established reference range (<0.03 µg/l), Troponin T banded at 0.03 µg/l was used in the Cox Regression model.



   Results
Top
 Abstract
 Introduction
 Subjects and methods
 Biochemical analyses
 Prospective data collection
 Statistical analyses
 Results
Discussion
 References
 
Of the 372 renal transplant recipients enrolled in this study, 239 (64%) participants were male, 71 (19%) participants were smokers, 52 (14%) participants were diabetic and 83 (22%) participants had a known history of vascular disease at enrolment. Characteristics of the renal transplant population enrolled in this study are shown in Table 1.


View this table:
[in this window]
[in a new window]

  		Table 1 Characteristics of the renal transplant recipients enrolled in this study

 
At enrolment 255 renal transplant recipients were prescribed an immunosuppression regimen that included a calcineurin inhibitor and 117 were prescribed a regimen that did not include a calcineurin inhibitor.

At follow-up 311 participants were alive and 61 (16.4%) participants had died. Of those who had died, 24 had died from a cardiovascular cause, 28 had died from a non-cardiovascular cause and for 9 renal transplant recipients cause of death could not be established.

The distribution of Troponin T for the population enrolled in the study ranged from less than 0.01–0.64 µg/l. Three hundred and forty-one participants had Troponin T less than or equal to 0.01 µg/l, 10 participants had a Troponin T of 0.02 µg/l and 21 had a Troponin T greater than or equal to 0.03 µg/l.

Troponin T correlated positively with age (r = 0.166 P = 0.001 Figure 1), but there was no significant relationship between Troponin T and total cholesterol (r = –0.071, P = 0.174), high density lipoprotein cholesterol (r = –0.079, P = 0.126), systolic blood pressure (r = 0.062, P = 0.231), diastolic blood pressure (r = –0.033, P = 0.533) or body mass index (r = –0.007, P = 0.898). Troponin T correlated significantly with estimated GFR (r = –0.134, P < 0.01), proteinuria (r = 0.152, P < 0.01) and high sensitivity C reactive protein (r = 0.132, P < 0.05, Figure 2).


Figure 1
View larger version (9K):
[in this window]
[in a new window]
[Download PowerPoint slide]
  		Fig. 1 Regression graph demonstrating the correlation between Troponin T and age (r = 0.166, P < 0.01).

 

Figure 2
View larger version (12K):
[in this window]
[in a new window]
[Download PowerPoint slide]
  		Fig. 2 Regression graph demonstrating the correlation between Troponin T and high sensitivity C reactive protein (r = 0.132, P < 0.05).

 
There was no significant difference in Troponin T concentration in those renal transplant recipients prescribed a calcineurin inhibitor as compared to those transplant recipients who were not prescribed a calcineurin inhibitor (P = 0.608). In those participants prescribed ciclosporin, there was no significant correlation between ciclosporin level and Troponin T concentration (P = 0.514).

The biological and biochemical characteristics of participants with an elevated Troponin T as compared to those with Troponin T within the reference range are shown in Table 2.


View this table:
[in this window]
[in a new window]

  		Table 2 Characteristics of the renal transplant recipients with a Troponin T less than or equal to 0.03 µg/l as compared to those with a Troponin T greater than 0.03 µg/l

 
As shown in Table 3, those renal transplant recipients who had died at follow-up were significantly older, more likely to be diabetic, had lower estimated GFR and were more likely to have had a cadaveric renal transplant and a history of vascular disease at enrolment as compared to those renal transplant recipients who were still alive at follow-up. Similarly, as shown in Figure 3, those renal transplant recipients who had died had significantly higher Troponin T levels as compared to those who were still alive at follow-up (0.01 (0.01, 0.02) vs 0.01 (0.01, 0.01) P < 0.001).


View this table:
[in this window]
[in a new window]

  		Table 3 Characteristics of the renal transplant recipients who had died at follow-up as compared to those who were still alive at follow-up

 

Figure 3
View larger version (7K):
[in this window]
[in a new window]
[Download PowerPoint slide]
  		Fig. 3 Distribution of Troponin T levels in those renal transplant recipients who had died at follow-up as compared to those who were alive at follow-up (P < 0.001).

 
Of the 351 transplant recipients with Troponin T less than 0.03 µg/l 49 (13.9%) had died at follow-up, while 12 of the 21 (57.1%) participants with a Troponin T greater than or equal to 0.03 µg/l had died at follow-up (P < 0.001). Those renal transplant recipients with a Troponin T concentration greater than or equal to 0.03 µg/l were significantly more likely to have died from a cardiovascular cause rather than from a non-cardiovascular cause (P < 0.001).

In Kaplan-Meier analysis, a Troponin T level above the upper reference range (i.e. greater than or equal to 0.03 µg/l) was a significant predictor of all-cause mortality (P < 0.001, Figure 4). As shown in Figures 5 and 6 respectively, a Troponin T greater than or equal to 0.03 µg/l was a significant predictor of both cardiovascular mortality (P < 0.001) and non-cardiovascular mortality (P = 0.0137).


Figure 4
View larger version (12K):
[in this window]
[in a new window]
[Download PowerPoint slide]
  		Fig. 4 Survival curve for renal transplant recipients stratified by Troponin T level for all-cause mortality (Kaplan-Meier analysis with log rank test, P < 0.001).

 

Figure 5
View larger version (11K):
[in this window]
[in a new window]
[Download PowerPoint slide]
  		Fig. 5 Survival curve for renal transplant recipients stratified by Troponin T level for cardiovascular death (Kaplan-Meier analysis with log rank test, P < 0.001).

 

Figure 6
View larger version (11K):
[in this window]
[in a new window]
[Download PowerPoint slide]
  		Fig. 6 Survival curve for renal transplant recipients stratified by Troponin T level for non-cardiovascular death (Kaplan-Meier analysis with log rank test, P = 0.0137).

 
In Cox Regression analysis Troponin T banded at 0.03 µg/l remained a significant predictor of mortality (P < 0.001) following adjustment for traditional cardiovascular risk factors (Table 4).


View this table:
[in this window]
[in a new window]

  		Table 4 The results of Kaplan-Meier and Cox Regression survival analysis stratified by Troponin T level

 
Renal function and high sensitivity C reactive protein have been identified as predictors of mortality in the general population and in patients with chronic kidney disease. Therefore given the correlation demonstrated between estimated GFR, high sensitivity C reactive protein and Troponin T in the transplant population described in this study, Cox Regression analysis was performed following adjustment for estimated GFR and high sensitivity C reactive protein. As highlighted in Table 4, elevated Troponin T at baseline remained a significant predictor of mortality even after adjustment for estimated GFR (P < 0.001) and high sensitivity C reactive protein (P < 0.001) and a Troponin T greater than or equal to 0.03 µg/l remained a significant predictor of mortality following adjustment for both estimated GFR and high sensitivity C reactive protein (P < 0.001). Troponin T remained a significant predictor of mortality following adjustment for traditional cardiovascular risk factors and the non-traditional risk factors haemoglobin, serum phosphate and parathormone (Table 4).



   Discussion
Top
 Abstract
 Introduction
 Subjects and methods
 Biochemical analyses
 Prospective data collection
 Statistical analyses
 Results
 Discussion
References
 
Cardiovascular disease remains the leading cause of death in renal transplant recipients, but traditional risk equations have been shown to consistently underestimate the risk of cardiovascular disease in this population [12]. Research has focused on the assessment of other biochemical markers as predictors of cardiovascular risk and mortality in patients with chronic kidney disease.

Numerous studies [5–11] have shown that increased Troponin T is a predictor of outcome in patients with end-stage renal disease. However, until now the significance of elevated Troponin T levels in renal transplant recipients has not been defined. The results of our study are the first to show that Troponin T is a strong independent predictor of all-cause mortality in patients with a renal transplant.

As one would expect in a group of stable asymptomatic renal transplant recipients, Troponin T levels at baseline were skewed; 94% of participants had Troponin T within the normal range and 6% had Troponin T above the upper reference interval. Although there were a small number of patients with an elevated Troponin T at baseline, there were significantly more deaths in this group at follow-up as compared to the group of participants with Troponin T within the reference range. Interestingly, those renal transplant recipients with an elevated Troponin T were significantly more likely to have died from a cardiovascular cause.

Univariate analysis indicated that Troponin T greater than or equal to 0.03 µg/l was a significant predictor of all-cause mortality. Furthermore, in subgroup analysis although Troponin T was a significant predictor of both cardiovascular and non-cardiovascular mortality, a Troponin T greater than or equal to 0.03 µg/l was a stronger predictor of cardiovascular mortality.

In multivariate Cox Regression analysis, Troponin T was strongly predictive of all-cause mortality independent of traditional risk factors, non-traditional risk factors (haemoglobin, serum phosphate and parathormone), renal function (estimated GFR) and high sensitivity C reactive protein.

Elevated Troponin T is strongly associated with traditional cardiovascular risk factors [3]. However, in the population described in this study, Troponin T correlated positively with age but did not correlate significantly with blood pressure, total cholesterol or high density lipoprotein cholesterol. Similarly, although patients with Troponin T greater than 0.03 µg/l were significantly older, there was no significant difference in blood pressure, lipid profile, diabetes or smoking history as compared to those participants with a Troponin T within the reference range.

Elevated Troponin T concentrations are not uncommon in patients with chronic kidney disease and the significance of raised Troponin T levels in this population is debated. However, the results of this study demonstrated that those renal transplant recipients with an elevated Troponin T were significantly more likely to have a history of vascular disease at enrolment and were significantly more likely to have died, particularly of a cardiovascular death, as compared to those with a Troponin T within the laboratory reference range.

The possibility that increased Troponin T concentrations in patients with chronic kidney disease reflect decreased clearance or analytical interference from uraemic serum seems unlikely on the basis of study results which have shown no difference between pre- and post-dialysis concentrations [1,13] and the observation that Troponin T is not universally elevated amongst uraemic patients. In our study, although there was a correlation between Troponin T and estimated GFR it does not prove a causal relationship and crucially Troponin T remained a significant predictor of mortality after adjustment for renal function.

Proteinuria is considered to represent the renal expression of a generalised disorder characterised by increased vascular permeability [14] and to act as a marker of endothelial dysfunction [15]. Similarly, high sensitivity C reactive protein has been identified as a prognostic biomarker and promoter of vascular disease [16].

In our study, those renal transplant recipients with elevated Troponin T levels had significantly more proteinuria and significantly increased high sensitivity C reactive protein levels as compared to those with Troponin T within the reference range. Similarly, in correlation analysis Troponin T correlated positively with proteinuria and high sensitivity C reactive protein. These findings support a role for inflammation and endothelial dysfunction as key mechanisms of myocardial injury in patients with a renal transplant. It can be hypothesised that the level of Troponin T reflects the burden of subclinical inflammation and endothelial dysfunction. Analysis of further parameters of inflammation and endothelial function, such as interleukin-6 and endothelin could help establish if this hypothesis were true.

Elevated Troponin T in patients with renal failure is, therefore, likely to be multifactorial in origin and may be caused by coronary artery stenosis, cardiac dysfunction, left ventricular hypertrophy or cardiac microinfarctions [17]. Nevertheless, whatever the mechanism for Troponin T release, elevation of Troponin T is indicative of myocardial damage and the results of this study are the first to show that an elevated Troponin T level is a strong independent predictor of all-cause mortality in patients with a renal transplant.

Troponin T, therefore, represents a powerful tool in the risk stratification of renal transplant patients and may enable the identification of transplant recipients who would benefit from more invasive cardiac investigation and intensive treatment of cardiovascular risk factors. One may hypothesise that in asymptomatic renal transplant recipients an elevated Troponin T level reflects subclinical myocardial injury, as a consequence of endothelial dysfunction, inflammation and vascular calcification [18], which contributes significantly to the risk of death.

In conclusion, the clinical significance of elevated Troponin T in patients with renal disease has been much debated. However, the results from this study are compelling and have shown that in the patients with a renal transplant the Troponin T concentration is a strong predictor of all-cause and cardiovascular mortality. Troponin T, therefore, represents a promising biochemical marker that is readily available in clinical practice that will enable risk stratification in renal transplant recipients and identify those who are most likely to benefit from aggressive cardiovascular risk factor modification.



   Acknowledgments
 
Dr G.C. and Dr R.C. were supported by Northern Ireland Kidney Research Fellowships. We would like to thank the research nurses for their help with patient recruitment, Mr Colin Craig and the Primary Care Physicians for their assistance in the collection of mortality data, Dr Chris Patterson for his statistical advice and the renal transplant patients, who gave generously of their time and without whom, this research would not have been possible.

Conflict of interest statement. Dr Grainne Connolly and Dr Ronan Cunningham were supported by Northern Ireland Kidney Research Fellowship Funds. This was the only source of funding and the authors declare no conflict of interest.



   References
Top
 Abstract
 Introduction
 Subjects and methods
 Biochemical analyses
 Prospective data collection
 Statistical analyses
 Results
 Discussion
 References
 

  1. 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) 106:118–123.[Web of Science][Medline]
  2. Wood GN, Keevil B, Gupta J, et al. Serum troponin T measurement in patients with chronic renal impairment predicts survival and vascular disease: a 2 year prospective study. Nephrol Dial Transplant (2003) 18:1610–1615.[Abstract/Free Full Text]
  3. Iliou MC, Fumeron C, Benoit MO, 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) 16:1452–1458.[Abstract/Free Full Text]
  4. deFilippi C, Wasserman S, Rosanio S, et al. Cardiac troponin T and C-reactive protein for predicting prognosis, coronary atherosclerosis, and cardiomyopathy in patients undergoing long-term hemodialysis. JAMA (2003) 290:353–359.[Abstract/Free Full Text]
  5. Porter GA, Norton T, Bennett WB. Troponin T, a predictor of death in chronic haemodialysis patients. Eur Heart J (1998) 19:N34–37.[Web of Science][Medline]
  6. Stolear JC, Georges B, Shita A, Verbeelen D. The predictive value of cardiac troponin T measurements in subjects on regular haemodialysis. Nephrol Dial Transplant (1999) 14:1961–1967.[Abstract/Free Full Text]
  7. Ooi DS, Zimmerman D, Graham J, Wells GA. Cardiac troponin T predicts long-term outcomes in hemodialysis patients. Clin Chem (2001) 47:412–417.[Abstract/Free Full Text]
  8. Dierkes J, Domrose U, Westphal S, et al. Cardiac troponin T predicts mortality in patients with end-stage renal disease. Circulation (2000) 102:1964–1969.[Abstract/Free Full Text]
  9. Deegan PB, Lafferty ME, Blumsohn A, et al. Prognostic value of troponin T in hemodialysis patients is independent of comorbidity. Kidney Int (2001) 60:2399–2405.[CrossRef][Web of Science][Medline]
  10. Fernandez-Reyes MJ, Mon C, Heras M, et al. Predictive value of troponin T levels for ischemic heart disease and mortality in patients on hemodialysis. J Nephrol (2004) 17:721–727.[Web of Science][Medline]
  11. Needham DM, Shufelt KA, Tomlinson G, et al. Troponin I and T levels in renal failure patients without acute coronary syndrome: a systematic review of the literature. Can J Cardiol (2004) 20:1212–1218.[Web of Science][Medline]
  12. Kasiske BL, Chakkera HA, Roel J. Explained and unexplained ischemic heart disease risk after renal transplantation. J Am Soc Nephrol (2000) 11:1735–1743.[Abstract/Free Full Text]
  13. Lowbeer C, Ottosson-Seeberger A, Gustafsson SA, et al. Increased cardiac troponin T and endothelin-1 concentrations in dialysis patients may indicate heart disease. Nephrol Dial Transplant (1999) 14:1948–1955.[Abstract/Free Full Text]
  14. Paisley KE, Beaman M, Tooke JE, et al. Endothelial dysfunction and inflammation in asymptomatic proteinuria. Kidney Int (2003) 63:624–633.[CrossRef][Web of Science][Medline]
  15. Hillege HL, Fidler V, Diercks GF, et al. Urinary albumin excretion predicts cardiovascular and noncardiovascular mortality in general population. Circulation (2002) 106:1777–1782.[Abstract/Free Full Text]
  16. Labarrere CA, Zaloga GP. C-reactive protein: from innocent bystander to pivotal mediator of atherosclerosis. Am J Med (2004) 117:499–507.[CrossRef][Web of Science][Medline]
  17. De Zoysa JR. Cardiac troponins and renal disease. Nephrology (Carlton) (2004) 9:83–88.[CrossRef][Medline]
  18. Jung HH, Ma KR, Han H. Elevated concentrations of cardiac troponins are associated with severe coronary artery calcification in asymptomatic haemodialysis patients. Nephrol Dial Transplant (2004) 19:3117–3123.[Abstract/Free Full Text]
Received for publication: 2. 1.07
Accepted in revised form: 20. 9.07


Add to CiteULike CiteULike   Add to Connotea Connotea   Add to Del.icio.us Del.icio.us    What's this?


This article has been cited by other articles:


Home page
 Nephrol Dial TransplantHome page
G. R. Shroff and B. L. Kasiske
Troponin T is an independent predictor of mortality in renal transplant recipients
Nephrol. Dial. Transplant., August 1, 2008; 23(8): 2707 - 2707.
[Full Text] [PDF]

Home page
 Nephrol Dial TransplantHome page
G. Connolly
Reply
Nephrol. Dial. Transplant., August 1, 2008; 23(8): 2707 - 2708.
[Full Text] [PDF]

This Article
Right arrow Abstract Freely available
Right arrow FREE Full Text (PDF) Freely available
Right arrow All Versions of this Article:
23/3/1019    most recent
gfm738v1
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Services
Right arrow Email this article to a friend
Right arrow Similar articles in this journal
Right arrow Similar articles in ISI Web of Science
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Add to My Personal Archive
Right arrow Download to citation manager
Right arrow Search for citing articles in:
ISI Web of Science (3)
Right arrowRequest Permissions
Right arrow Disclaimer
Google Scholar
Right arrow Articles by Connolly, G. M.
Right arrow Articles by Maxwell, A. P.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Connolly, G. M.
Right arrow Articles by Maxwell, A. P.
Social Bookmarking
Add to CiteULike   Add to Connotea   Add to Del.icio.us  
What's this?