Elevated cardiac troponin T in peritoneal dialysis patients is associated with CRP and predicts all-cause mortality and cardiac death
Christian Löwbeer1,,
Alberto Gutierrez2,
Sven A. Gustafsson1,
Rolf Norrman2,
Johan Hulting3 and
Astrid Seeberger2
1 Division of Clinical Chemistry, Department of Medical Laboratory Sciences and Technology,
2 Division of Renal Medicine, Department of Clinical Science, Karolinska Institutet at Huddinge University Hospital and
3 Department of Medicine, Karolinska Institutet at Södersjukhuset, Stockholm, Sweden
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Abstract
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Background. Cardiac troponin T (cTnT) is a highly sensitive and specific marker of myocardial damage. In sera from patients with end-stage renal disease, cTnT may be elevated without other signs of acute myocardial injury. It has been shown that elevated cTnT in haemodialysis patients is associated with poor prognostic outcome. The aim of the present study was to test the hypothesis that elevated cTnT in a single serum sample from peritoneal dialysis (PD) patients is of prognostic importance.
Methods. Blood samples were taken from 26 randomly selected PD patients without signs of acute myocardial ischaemia. Sera were analysed for: cTnT with the second generation TnT ELISA on ES 300; cardiac troponin I (cTnI) with Opus Plus; and for creatine kinase-MB (CKMB) mass and C-reactive protein (CRP). After 4 years, clinical outcomes were evaluated by chart review. The influence on survival was tested with KaplanMeier analysis and Cox's proportional regression analysis.
Results. Concentrations of cTnT
0.04 µg/l and CRP
10 mg/l were strong predictors of all-cause mortality in univariate analysis. Twelve out of 14 patients with cTnT
0.04 µg/l died compared with three out of 12 with cTnT <0.04 µg/l. Other factors that influenced survival were age and the presence of ischaemic heart disease (IHD). There was a significant positive correlation between cTnT and CRP, and between cTnT and age. Cardiac troponin T was an independent predictor compared with age but not compared with CRP and IHD. Neither cTnI nor CKMB mass concentrations were related to survival.
Conclusion. Elevated serum concentrations of cTnT significantly predicted poor outcome and there was a correlation between cTnT and CRP concentrations in samples from PD patients. Cardiac troponin I and CKMB mass had no prognostic value.
Keywords: cardiac troponin; C-reactive protein; creatine kinase isoenzymes; peritoneal dialysis; survival
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Introduction
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The poor prognosis of patients with end-stage renal disease (ESRD) is due greatly to the high incidence of cardiovascular disease, accounting for about half of all deaths. Twenty to thirty per cent of cardiac deaths in these patients are caused by myocardial infarction [1]. Cardiac troponin T (cTnT) measured in serum or plasma is a highly sensitive and specific marker of acute myocardial damage and a predictor of adverse outcome in non-uraemic patients with unstable coronary disease [2]. However, the use of cTnT has been questioned in ESRD patients since cTnT concentrations may be elevated without other signs of acute myocardial damage [3,4]. The mechanism behind the increased cTnT concentration is unclear, although associations have been shown with age, diabetes mellitus and coronary artery disease [5]. Some studies have shown that cTnT predicts cardiovascular mortality as well as all-cause mortality in renal patients treated with haemodialysis (HD) [6,7], whereas others have reported no association with outcome [8,9]. The role of cTnT as a prognostic marker in peritoneal dialysis (PD) patients has not yet been investigated. Thus the value of cTnT determinations in patients with renal failure has not been clearly established.
In addition, increased concentrations of C-reactive protein (CRP), a marker of inflammation, has been shown to be associated with elevated serum cTnT and to predict outcome in HD patients [10]. In PD patients, CRP has been shown to be predictive of myocardial infarction [11] and all-cause mortality [12]. To our knowledge, correlations between CRP and cTnT have not been studied in PD patients. Therefore, the main aim of the present study was to investigate the prognostic value of cTnT and CRP in a single serum sample withdrawn from PD patients. In addition, we studied whether other markers of myocardial injury [cardiac troponin I (cTnI), creatine kinase-MB (CKMB) mass and creatine kinase (CK)] could be used as predictors of mortality.
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Subjects and methods
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Patients and protocol
Twenty-six patients, 3280 years old, treated with chronic ambulatory peritoneal dialysis (CAPD), were randomly selected at one dialysis centre. The patients were included during a 1 month period out of a total of 50 patients treated with CAPD at the time. Exclusion criteria were acute myocardial infarction within 3 weeks prior to blood sampling and/or clinical symptoms of inflammation. For analysis of serum cTnT, cTnI, CKMB mass, CK and CRP, peripheral venous blood was collected in tubes without additives. Serum CRP, CKMB mass and CK were determined immediately. Serum for cTnT assay was stored at -20°C and analysed within 24 h. Serum specimens for cTnI and creatinine were stored at -70°C and analysed in a batch manner. Clinical characteristics at inclusion in the study, including serum concentrations of parathyroid hormone (Incstar N-tact PTH), albumin (Behring Nephelometer Analyzer) and blood haemoglobin (Technicon H2), were collected from patient files. Chronic ischaemic heart disease (IHD) was defined as a history of angina pectoris and/or previous myocardial infarction. Four years after blood sampling, outcome was investigated by chart review. Ten patients had undergone renal transplantation. Three of these had also been treated with haemodialysis for some period. Six patients had switched from PD to HD. Fifty-three per cent of the causes of death were based on post-mortem autopsy. Cardiac death was defined as acute myocardial infarction, sudden death or congestive heart failure. The study protocol was approved by the local ethics committee and the subjects were informed of the purpose of the study before giving their voluntary consent. The frequency of elevated cardiac markers and the associations between these and some clinical variables in this population have been reported previously [13].
Biochemical assays
Cardiac troponin T was determined with the second generation troponin T ELISA (Enzymun-Test Troponin-T) on ES 300 system (Boehringer Mannheim GmbH, Mannheim, Germany). This assay uses the two cardiac-specific monoclonal antibodies M11.7 and M7 [14]. The detection limit was 0.04 µg/l. Cardiac troponin I was measured with the Opus Troponin I assay (Behring Diagnostics, Westwood, MA, USA) performed on the Opus Plus analyser, with a detection limit of 0.5 µg/l. Creatine kinase-MB mass was analysed by Microparticle Enzyme Immunoassay (MEIA) technology with AxSYM system (Abbott Diagnostics, Abbott Park, IL, USA). Serum CRP, CK and creatinine were measured with dry chemistry using Ektachem 950ICR System (Johnson & Johnson Clinical Diagnostics, Inc., Rochester, NY, USA). The detection limit for CRP was 7 mg/l. The total imprecisions (CV%) of the assays were: 8.0% at 0.16 µg/l for cTnT; 8.4% at 7.1 µg/l for cTnI; 8.3% at 3.8 µg/l for CKMB mass; 8.6% at 192 U/l for CK; and 14% at 21 mg/l for CRP.
The reference limits used in clinical routine were: cTnT <0.10 µg/l, cTnI <2.0 µg/l, CKMB mass <5 µg/l, CK (males) <174 U/l, CK (females) <144 U/l and CRP <10 mg/l.
Statistical analysis
Most quantitative variables were not normally distributed and therefore values are given as median and interquartile range. Differences between unpaired quantitative data were analysed by MannWhitney U-test. KaplanMeier curves were used to describe the cumulative survival based on elevated cTnT and significance was tested with the log-rank test. The influence of different parameters on survival was analysed with Cox's proportional hazard regression, and to test if cTnT was an independent risk marker cTnT and other covariates were entered simultaneously into the regression. The relationship between elevated cTnT and CRP, and differences between other nominal variables were analysed with Fisher's exact two-tailed test. Correlations were tested with Spearman rank correlation (
=correlation coefficient). Statistical significance was defined as P<0.05. Statistics were performed using Statistica 5.5 (Stat Soft, Inc., USA).
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Results
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The basal clinical characteristics of all patients, survivors and non-survivors, are shown in Table 1
. During the 48 month follow-up period, 15 of the 26 patients died. The causes of death were: acute myocardial infarction and sudden death (n=8), congestive heart failure (n=3), leukaemia, sepsis, cerebral infarction and pulmonary oedema. Survivors had lower serum concentrations of cTnT (P<0.01) and CRP (P<0.05) than non-survivors (Table 2
). Three of 12 patients with cTnT <0.04 µg/l died compared with 12 of 14 with cTnT
0.04 µg/l (P<0.01). There was a negative correlation between serum cTnT concentration and survival time (
=-0.76, P<0.0001). Five patients were treated in hospital for acute myocardial infarction, angina pectoris or heart failure during the period. There was no difference in cTnT between these five and event-free patients. Using a discriminator of
0.10 µg/l for cTnT and
10 mg/l for CRP, there was a close relationship between these two analytes (P<0.0001), as shown in Table 3
. There was a positive correlation between cTnT and CRP (
=0.67, P<0.001).
The cumulative survival was lower for patients with an initial serum cTnT of
0.04 µg/l (P<0.001) (Figure 1
) and the cumulative proportion of cardiac deaths was higher for these patients (P<0.01). Also, when using the cut off
0.10 µg/l, cTnT significantly influenced survival (P<0.001); all eight patients with cTnT
0.10 µg/l died. In Table 4
, cTnT is listed together with other variables that influenced survival in univariate analysis: serum CRP, albumin, IHD and age. Survival was not influenced by cTnI, CKMB mass, CK, haemoglobin, parathyroid hormone, duration of renal disease or duration of CAPD. When tested multivariately together with albumin and age, both cTnT
0.04 µg/l (P<0.05) and CRP
10 mg/l (P<0.01) were independent risk markers for death. Serum cTnT and CRP together strongly influenced survival (P<0.001) but the separate P-values did not reach significance (P=0.068 for cTnT and P=0.094 for CRP). When comorbidity was entered into the regression analysis, cTnT
0.04 µg/l was still an independent predictor of all-cause mortality (P<0.05), whereas congestive heart failure (P=0.12), atrial fibrillation (P=0.12) and IHD (P=0.16) were not. When patients who underwent renal transplantation were excluded, cTnT still influenced survival (n=16, P<0.01), whereas the influence of CRP was near significant (P=0.05). Patients with a history of IHD had higher cTnT than patients without IHD [0.15 (0.080.46) vs <0.04 (<0.040.08) µg/l; P<0.05]. There was no significant difference in CRP concentration between these groups [<7 (<723) vs <7 (<78) mg/l; P=0.22].

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Fig. 1. KaplanMeier survival analysis curves according to serum concentrations of cTnT in samples collected from peritoneal dialysis patients at time zero. Open circles, cTnT <0.04 µg/l (n=12); open squares, cTnT 0.04 µg/l (n=14). ***P<0.001 compared with the other survival curve.
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Transplanted patients had lower cTnT than those not transplanted [<0.04 (<0.040.06) vs 0.12 (<0.040.24) µg/l; P<0.05]. Patients treated with angiotensin-converting enzyme (ACE) inhibitors or angiotensin II-receptor antagonists (n=7) had lower serum cTnT than patients without these medications (n=19) [<0.04 (<0.04<0.04) vs 0.07 (<0.040.18) µg/l; P<0.05]. No particular medication (listed in Table 1
) had prognostic importance.
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Discussion
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The main finding of the present study was a significant relationship between poor long-term outcome and elevated serum concentrations of cTnT and CRP in a single sample from PD patients. We also showed a strong association between cTnT and CRP.
Patients with cTnT values
0.04 µg/l at inclusion had higher risk for all-cause and cardiac death during the 48 month follow-up. The relationship between elevated cTnT and increased mortality has been shown for HD patients [57,10] but has not been reported using samples from PD patients.
The pathophysiological basis and the biochemical processes underlying the elevated cTnT concentrations in chronic renal failure are unclear, although several hypotheses have been proposed. The design of the present study does not allow us to define the mechanisms behind the increased serum cTnT. However, we have shown earlier that elevated cTnT levels were associated with left ventricular hypertrophy (LVH) in HD patients [13]. Left ventricular hypertrophy is known to be associated with increased mortality. The pathogenesis of LVH has been linked to the activation of the reninangiotensin system and treatment of patients with chronic renal failure with ACE inhibitors has been shown to result in regression of left ventricular mass index [15]. Interestingly, in the present study, patients treated with ACE inhibitors or angiotensin II-receptor antagonists had lower serum cTnT than non-treated patients. We did not perform echocardiography in the study patients so we cannot draw any conclusions regarding the influence of LVH on cTnT and mortality in this population.
Another explanation for the association between cTnT and mortality might be that cTnT is more sensitive than other cardiac markers for the detection of undiagnosed myocardial pathologies, which increase the risk of death. This has been shown for cTnT compared with cTnI measured with the AxSYM assay [16]. There are a number of papers indicating an association between elevated cTnT and cardiac disease other than acute myocardial infarction in HD patients [5,13,17,18]. In the present study, PD patients with IHD had significantly higher serum cTnT than patients without IHD. This strengthens the hypothesis that elevated cTnT in ESRD patients reflects cardiac disease.
It is possible that cTnT is so sensitive that it detects cardiac disease that is undetectable with other cardiac markers. In renal failure, cTnT might be even more sensitive in detecting minor myocardial damage as compared with patients with normal renal function. It has been speculated that there may be retention of proteolytic degradation products of cTnT in dialysis patients and that these degradation products are detected by the cTnT assay [19]. The increased half-life would then amplify the serum concentration of cTnT in cases with minor ongoing myocardial damage, whatever the cause.
It has been suggested that the myopathy associated with ESRD may induce the expression of cTnT in replicating skeletal muscle. McLaurin et al. [20] reported evidence of cTnT expression in skeletal muscle of dialysis patients. However they did not use the same antibodies (M11.7 and M7) that are used in the second and third generation cTnT assay. On the contrary, in another study there was no evidence of cTnT expression in skeletal muscle biopsies of ESRD patients [21]. Furthermore, Ricchiuti et al. [22] showed that cardiac TnT isoforms expressed in renal diseased skeletal muscle will not cause false-positive results by using the M11.7 and M7 antibodies. Therefore, it is most likely that serum cTnT in PD patients, as measured by the second generation cTnT assay, originates from the heart. Thus, our data suggest a high prevalence of myocardial disease in these patients.
Our finding of lower cTnT in patients who later received a renal transplant are consistent with the data of Ooi et al. [5], who found that only 3% of HD patients with cTnT
0.10 µg/l were transplanted. This may indicate that increased serum cTnT is associated with poor health in ESRD.
In addition, we found an association between serum cTnT and the inflammatory marker CRP. To our knowledge this has not been shown before in PD patients, although associations between cTnT and CRP have been reported in HD patients [10]. We found that CRP predicted mortality in PD patients, which is in accordance with previous studies [12,23]. In another study, CRP predicted myocardial infarction but not all-cause mortality [11]. It is known that loss of renal function leads to changes in serum/plasma composition which are associated with vascular disease, and signs of malnutrition and inflammation are common in dialysis patients. Furthermore, it is recognized that acute-phase proteins and cytokines are powerful markers for cardiovascular risk both in the general population [24,25] and in ESRD [26,27]. Chronic inflammation is believed to cause accelerated arteriosclerosis resulting in cardiovascular disease and increased risk for death [28]. Furthermore, CRP per se may be a mediator of myocardial injury [29]. Therefore, the correlation between CRP and cTnT in the present study could be explained by the tendency shown by both markers to increase in the presence of cardiac disease. Notably, CRP together with cTnT have been shown to be risk markers in non-uraemic patients with unstable angina pectoris [30]. However, the association between CRP and cardiovascular disease has been questioned since it was demonstrated that clinically apparent cardiovascular disease did not predict high CRP levels in PD patients [31]. In the present study, serum CRP
10 mg/l was associated with an increased mortality rate. However, CRP was not significantly higher in patients with than without IHD. This is in accordance with the finding that many patients with known severe atherosclerotic disease have normal CRP levels [31]. Furthermore, the cause of inflammation in ESRD is likely to be multifactorial. However, due to limitations of the study (a relatively small study population, diagnoses based on medical history and inability to measure CRP concentrations <7 mg/l) we cannot draw any firm conclusions regarding associations between CRP and myocardial disease.
When elevated serum cTnT and CRP were tested together in regression analysis, they strongly predicted all-cause mortality but the two analytes were not independent of each other. There was also a positive correlation between the concentrations of cTnT and CRP. These findings suggest an association between cTnT and ongoing inflammation in PD patients.
Cardiac troponin I measured with the Opus Plus analyser gave no prognostic information since only one of 26 patients had a detectable concentration (data not shown). This is important since both cTnI measured with the Opus Magnum device and cTnT provided prognostic information regarding cardiac death and acute myocardial infarction in non-uraemic patients with suspected unstable coronary artery disease [32]. In a study on HD patients with no complaints of chest pain, three out of 48 had elevated cTnI with the Opus method and all three suffered an adverse outcome [33]. Other studies have shown that Access troponin I (Sanofi Diagnostics Pasteur) was slightly elevated in 17% of HD patients [34] and that cTnI measured with the Stratus II analyser (Dade) appeared to predict cardiac complications in HD patients [35]. In another study, Stratus II cTnI and Opus Plus cTnI were not predictive of outcome [8]. Thus, at present it is not possible to draw any general conclusion regarding the predictive value of cTnI in ESRD. Each cTnI assay uses unique antibodies, which may explain their different properties when analysing cTnI in samples from uraemic patients.
The present data contribute to the reports indicating that serum cTnT and CRP may be an aid in risk stratification of dialysis patients. However, to choose the appropriate investigations and treatments to reduce these risks, further studies are needed to clarify the pathological basis for elevated cardiac troponins in ESRD patients.
In summary, elevated serum cTnT in samples from PD patients predicted death and was associated with elevated serum CRP. The present data support the hypothesis that cTnT is associated with poor outcome in ESRD and indicate that cTnT may be used as a risk marker in PD patients.
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Acknowledgments
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We thank the staff of the Department of Clinical Chemistry, Södersjukhuset, Stockholm, for their helpful technical support. This work was supported by grants from The Swedish Association for Renal Diseases.
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Notes
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Correspondence and offprint requests to: Christian Löwbeer MD, Department of Clinical Chemistry, Huddinge University Hospital, S-141 86 Stockholm, Sweden. Email: christian.lowbeer{at}chemlab.hs.sll.se 
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Received for publication: 18. 1.02
Accepted in revised form: 30. 7.02