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Cardiac Troponin T Predicts Long-Term Outcomes in Hemodialysis Patients

¹ Divisions of Biochemistry and
² Nephrology, Ottawa Hospital–Civic Campus, 1053 Carling Ave., Ottawa, ON K1Y 4E9 Canada.

³ Departments of Epidemiology and Community Medicine,
⁴ Pathology, and
⁵ Medicine, University of Ottawa, Ottawa, ON K1H 8M5, Canada.
^a Address correspondence to this author at: Division of Biochemistry, Department of Pathology and Laboratory Medicine, Ottawa Hospital–Civic Campus, 1053 Carling Ave., Ottawa, ON K1Y 4E9 Canada. Fax 613-761-5401; e-mail dsooi{at}ottawahospital.on.ca.

	Abstract

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Background: Increased plasma troponin T (cTnT), but not troponin I (cTnI), is frequently observed in end-stage renal failure patients. Although generally considered spurious, we previously reported an associated increased mortality at 12 months.

Methods: We studied long-term outcomes in 244 patients on chronic hemodialysis for up to 34 months, correlating the outcomes to plasma cTnT in routine predialysis samples. In addition, subsequent plasma samples at least 1 year later and within 6 months of data analysis were available in 97 patients and were used to identify patients with increasing plasma cTnT. The endpoints used were death and new or worsening coronary, cerebro-, and peripheral vascular disease and neuropathy.

Results: Transplantation occurred more frequently in patients with low initial cTnT: 31%, 13%, and 3% in the groups with cTnT <0.010, 0.010–0.099, and 0.100 µg/L, respectively. In the same groups, total deaths occurred in 6%, 43%, and 59% and cardiac deaths in 0%, 14%, and 24% of patients. In patients with follow-up samples, the group with increasing cTnT had a significantly increased death (relative risk, 2.0; P = 0.028). The increase was mainly in cardiac and sudden deaths.

Conclusions: Higher plasma cTnT predicts long-term all-cause mortality in hemodialysis patients, even at concentrations <0.100 µg/L, as does an increasing cTnT concentration over time.

	Introduction

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Increased plasma cardiac troponin T (cTnT)¹ (1)(2)(3)(4)(5), but not troponin I (cTnI) (4)(5), is frequently observed in end-stage renal disease (ESRD) patients without acute coronary disease. This unexplained increase has major clinical implications for these patients who are at high risk of ischemic heart disease, especially silent myocardial infarction. Many consider the increases spurious (6) because older immunohistochemical studies demonstrated the presence of cTnT in skeletal and diaphragmatic muscle (7)(8). However, a recent study (9) reported that the cardiac isoform in skeletal muscles of renal failure patients is structurally different from that in cardiac muscle and is not likely to be detected by the commercial assay.

We previously reported the pattern of plasma cTnT increases in 172 patients on chronic hemodialysis (10) and found that 29% of patients had plasma cTnT concentrations 0.1 µg/L (the recommended clinical threshold) and 10% had values 0.2 µg/L. Serum creatinine, dialysis adequacy, and duration in program were not associated with higher prevalence, but diabetes (57%), especially with multiple complications, and age were. The most intriguing finding was that coronary artery disease (CAD) did not appear to influence cTnT concentrations. At 1 year, we noted a marked increase in mortality in patients with increased cTnT (11). Surprisingly, death was attributable mainly to causes other than acute coronary events, and the correlation with increased mortality was significant mostly in patients traditionally at lower risk: those with no CAD or peripheral vascular disease (PVD), and nondiabetics. We followed this cohort for up to 34 months to confirm these findings.

	Materials and Methods

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The study was conducted in accordance with ethical standards of the institution. The initial 172 patients, recruited between August and September 1997, have been described previously (10). An additional 72 patients were recruited during February 1999. Patients received an average of 12 h of hemodialysis three times a week on a non-reprocessed semisynthetic or synthetic dialyzer. Routine predialysis plasma samples obtained from lithium heparinized blood were analyzed for cTnT on the Elecsys^® 1010 (Roche Diagnostics, Laval, Quebec, Canada), using the second-generation assay up to March 1999 and the third-generation assay from then on. Both assays have no cross-reactivity with skeletal troponin T. The day-to-day CV was 7.7% at 0.2 µg/L. In 97 patients, two or more values were obtained at least 1 year apart and within 6 months of data analysis.

Patients were grouped by plasma cTnT concentration, according to the initial value observed, into groups with 0.010, 0.010–0.049, 0.050–0.099, 0.100–0.199, and 0.200 µg/L cTnT. Increased cTnT values that were determined later to have been collected during an acute coronary event (based on clinical and additional laboratory data) were excluded. Patients were followed for death, new acute coronary events, PVD, cerebrovascular disease (CVD), neuropathy, and renal transplantation. Mortality and morbidity rates were calculated after the patients who had left the program or had undergone renal transplantation had been eliminated. Cause of death was based on clinical diagnosis in most cases. Cardiac status was determined by history of myocardial infarction or angina pectoris, or clinical assessment by a cardiologist as part of the work up for renal transplantation (including electrocardiography, echocardiography, exercise thallium scintigraphy, and angiography in a few patients). Patients with a past history of acute coronary syndromes or failed clinical testing were considered to have significant CAD.

Because many ESRD patients have subclinical neuropathy and PVD, an event was based on new symptoms necessitating a referral to a neurologist or vascular surgeon, respectively, or need for peripheral amputation in the latter. ² analysis for trend and the Fisher exact two-tail test were performed, and relative risks with 95% confidence intervals (95% CIs) were calculated using Epi Info, Ver. 6 (12). Statistical significance was defined as P <0.05. Further statistical analyses were done using the SAS program (13). Kaplan-Meier curves were used to describe the survival experience for groups based on cTnT, and difference in survival was assessed using the log-rank test. The effect of covariates that may influence cTnT values were adjusted using the Cox proportional hazards model.

	Results

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Patient demographics are summarized in Table 1 . The group with initial plasma cTnT <0.010 µg/L tended to be younger; thus, the etiology of ESRD was less likely from complications of diabetes mellitus and hypertension but more frequently from glomerulonephritis and congenital causes. This group had lower associated morbidities, especially CAD, CVD, and PVD. Duration in the dialysis program was not significantly different among the groups.

Outcomes based on initial cTnT are shown in Table 2 . Of the patients who left the program, one was lost to follow-up, and 14 of 16 joined nonhospital facilities. There was no significant difference for patient loss among the groups. There was a significant trend for renal transplantation (P = 0.014) in the groups with lower cTnT; only two (3%) patients with cTnT 0.1 µg/L were transplanted.

deaths
There were 87 deaths during the period of observation. Of the patients with initial plasma cTnT <0.01 µg/L (not detectable), only 1 of 27 (3%) patients died (of lung cancer) during this follow-up period. The ² analysis for trend was significant (P <0.001). Because the survival curves for the groups with initial plasma cTnT concentrations of 0.010–0.049 and 0.050–0.099 µg/L were similar, as were the curves for the groups with 0.100–0.199 and 0.200 µg/L cTnT, the groups were appropriately combined for further analysis. Repeat ² analysis for trend was again highly significant (P <0.00001). The relative risk for death in the 0.010–0.099 and 0.100 µg/L groups, when compared with the <0.010 µg/L group, was 7.3 (95% CI, 1.1–49; P <0.005) and 10.0 (95% CI, 1.5–68; P <0.001), respectively. The Kaplan-Meier survival curves for the three groups (shown in Fig. 1A ) were significantly different (P <0.005). This effect was present even after adjusting for the covariates of age, coexisting diabetes mellitus, and glomerulonephritis as etiology (P <0.001). Cause of death is shown in Table 3 . In contrast to our findings at 12 months, cardiac, rather than noncoronary, deaths were significantly increased with increasing cTnT.

View larger version (19K): [in this window] [in a new window]   Figure 1. Survival (A) and event-free survival (B) curves for the three groups based on cTnT concentrations at the beginning of the study. Dotted line, initial plasma cTnT concentration <0.010 µg/L; thin solid line, initial plasma cTnT concentration 0.010–0.099 µg/L; thick solid line, initial plasma cTnT concentration 0.100 µg/L.

In the 97 patients with subsequent samples at least 1 year from the initial sample and within 6 months of data analysis, 28 patients had died, 17 had new or worsening CAD, 2 had congestive heart failure (CHF), 5 suffered cerebrovascular events, 4 had worsening PVD, 2 had neuropathy, and 39 had no significant outcome. The pattern of subsequent cTnT for these various outcomes (shown in Fig. 2 ) again demonstrated the association of cTnT with mortality. Plasma cTnT concentrations increased >60% in 58% and 63% of cardiac and other death groups, respectively, and decreased concentrations (>60%) were seen in only 14% of those who died. The relative risk for death with increasing cTnT concentration was 2.0 (95% CI, 1.1–3.9; P = 0.028).

View larger version (27K): [in this window] [in a new window]   Figure 2. Changes in cTnT over time. , 30% increase in concentration; , no change (± 29%) or fluctuating concentration; , 30% decrease in concentration.

morbidity
Initial cTnT concentrations appeared to have no effect on subsequent development of CAD, CVD, PVD, or neuropathy (Table 2 ). However, a statistically significant increase in morbidity was found with increasing cTnT concentrations. Of those with deteriorating cardiac disease, 42% showed a >60% increase in cTnT, whereas only 27% of those who developed other morbidities (PVD, CVD, or neuropathy) and 36% of event-free survivors showed increasing cTnT. Kaplan-Meier curves (Fig. 1B ) for event-free survival (death and new or worsening CAD, CVD, PVD, CHF, or neuropathy) showed a significant difference between the groups based on initial cTnT (P <0.05), but this significance was no longer present when the covariates of age, diabetes mellitus, and glomerulonephritis were factored in, primarily because of the first two covariates.

	Discussion

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End-stage renal failure patients have high mortality, with cardiovascular causes accounting for almost one-half of deaths (14). Coexisting diabetes mellitus (14) and ischemic heart disease (14)(15), age, hypotension, hypoalbuminemia, and inadequacy of hemodialysis have also been shown to be associated with higher mortality.

There are conflicting reports regarding the relationship between increased cTnT and mortality. Some studies have shown no association (16)(17), whereas others have reported increased mortality (4)(5)(18)(19)(20)(21)(22). The duration of follow-up in these studies was 2 years or less and was based on smaller cohorts. In a recently published study on 102 hemodialysis patients over 2 years (22), a sevenfold increase in mortality was observed in patients with cTnT 0.1 µg/L. However, in a cohort of 98 patients followed for 1 year, Mockel et al. (17) were unable to demonstrate a relationship between cTnT and mortality. Our large cohort study, over a longer period, shows the predictive value of cTnT in patients with ESRD. In addition, the increased mortality associated with increasing cTnT over time further strengthens the suggestion that cTnT is indicative of underlying morbid processes.

The difference in survival was not attributable to coexisting diabetes mellitus. This is important information because it previously was shown that increased cTnT in ESRD was seen most frequently in diabetics (10), the group with the highest mortality among hemodialyzed patients. Although diabetes mellitus was a significant predictor of event-free survival, this was not surprising because most of the morbidities studied were associated with poor diabetic control.

The pathologic basis for cTnT in the serum of these patients is still unclear. It is difficult to explain the lack of an associated increase in cTnI. The commonly believed hypothesis of reexpression of the cardiac isoform in diseased skeletal muscle is not likely, for although cTnT isoforms can be present in diseased skeletal muscles, they differ from those in cardiac tissue and are not detectable with the pair of antibodies (M11.7 and M7) used in the commercial assay (9). In studies that compared the two troponins in ESRD (4)(5), acute coronary events were more frequent when both troponins were increased than when cTnT alone was increased. Two hypotheses could explain this. One hypothesis is that cTnT may be a more sensitive marker; thus, only patients with more severe CAD will have increases in cTnT. Our observation that even marginally increased cTnT is associated with mortality certainly supports this. However, we do not think this likely for two reasons. In acute coronary syndromes, both troponins show similar ability for risk stratification (23). In addition, one would expect that cTnI would be present, but in lower concentrations. Measurement in survivors in our cohort showed detectable cTnI in only a few patients (data not shown). Hence, we are left with the possibility that for patients with increased cTnT there are two groups: those with CAD where both troponins are increased, and those with some other pathologic basis for the increase in cTnT alone. The second hypothesis is based on the notion that CHF, a common complication in this group of patients, could be a possible basis for increased cTnT. The poorer prognosis of hypotensive or normotensive patients with increased cTnT at 1 year supports this (11). However, cTnT (24)(25) and cTnI (26) have both been shown to be predictive of poor outcomes in CHF. Although one could argue that cTnT may be more sensitive in CHF, our recent study has shown that the percentages of detectable troponin and the prognostic capability were similar for cTnT and the Abbott Diagnostics cTnI (27). Hence, CHF alone as the cause cannot explain the discordance between the two troponins.

One unifying hypothesis to consider is that two or more processes act to give rise to increased cTnT without associated increased cTnI. In renal failure, there may be circulating substances that modify troponins differently to affect either their clearance rate or reactivity in the analytical assay and thus produce discordance between the troponins. Hence, myocardial disease (ischemic or degenerative) is a prerequisite and explains the ability of plasma cTnT to provide risk stratification. Increasing concentrations over time, as observed in some of our patients who died, signify either progression of degenerative myocardial disease or frequent microinfarctions. In patients without such chemical modification of cTnT, such as those with acute coronary syndromes or CHF, the two troponins behave similarly. Studies on the circulating forms of troponins in ESRD patients will greatly increase our understanding of this interesting phenomenon.

Some of our findings were surprising. The first surprise was the correlation with cardiac mortality, not seen with the 1-year follow-up (11). Following on the above hypothesis, one could speculate that the higher rate of chemical modification in terminally ill patients requires only minimal cardiac disease for plasma cTnT to be increased; hence, cardiac events were disproportionately lower in the 1-year follow-up. The second surprise was the lack of correlation between cardiac morbidity and cTnT concentration. Although this may be explained partly by asymptomatic infarctions causing misclassification of cTnT class, one would still expect such patients to have accelerated progression of cardiac disease, again pointing to the interaction of synergistic factors.

One interesting, but not surprising, observation was the low rate of transplantation in patients with increased cTnT concentrations, pointing to the fact that poor health is associated with increased cTnT concentrations.

Although it is still generally believed that increased cTnT in ESRD is spurious, our study shows that it is associated with increased risk of morbidity and death. Even marginally increased concentrations, below the clinical threshold value of cTnT, were associated with increased morbidity and mortality in this group of ESRD patients. The use of troponins in risk stratification of patients with acute coronary syndromes is now widely accepted. With recent evidence from studies on CHF, ESRD, sepsis (28)(29), and other severe illnesses (29)(30), their clinical use may be broadened to include these clinical conditions.

	Acknowledgments

 
We wish to thank Roche Diagnostics, Canada, for providing us with analytical kits, and E. Yetiser for assistance in data analysis.

	Footnotes

 
Departments of ³ Epidemiology and Community Medicine, ⁴ Pathology, and ⁵ Medicine, University of Ottawa, Ottawa, ON K1H 8M5, Canada.

¹ Nonstandard abbreviations: cTnT and cTnI, cardiac troponin T and I; ESRD, end-stage renal disease; CAD, coronary artery disease; PVD, peripheral vascular disease; CVD, cerebrovascular disease; CI, confidence interval; and CHF, congestive heart failure.

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