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Serum cardiac biomarkers in patients with renal failure
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Serum cardiac biomarkers in patients with renal failure
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Literature review current through: Nov 2017. | This topic last updated: Jun 01, 2016.

INTRODUCTION — Cardiac biomarkers are used in conjunction with symptoms, electrocardiographic (ECG) changes, and cardiac imaging to diagnosis acute myocardial infarction (AMI) in patients with chronic kidney disease (CKD) [1]. Cardiac biomarkers are also used to predict short- and long-term adverse outcomes.

The principal cardiac biomarkers are cardiac troponin T (cTnT), cardiac troponin I (cTnI), and the MB isoenzyme of creatine kinase (CK-MB). (See "Troponin testing: Clinical use".)

This topic reviews the clinical use of cardiac troponins and CK-MB in patients with CKD. The use of these biomarkers in patients with normal renal function is discussed separately. (See "Troponin testing: Clinical use".)

The use of other enzymes in patients with CKD is discussed separately. (See "Serum enzymes in patients with renal failure".)

The risk of coronary artery disease (CAD) among dialysis and nondialysis patients with CKD is discussed separately. (See "Chronic kidney disease and coronary heart disease" and "Clinical manifestations and diagnosis of coronary heart disease in end-stage renal disease (dialysis)".)

DIAGNOSIS OF ACUTE MYOCARDIAL INFARCTION

Troponins — Cardiac troponins T and I (cTnT and cTnI) are the preferred biomarkers for the diagnosis of myocardial injury for all patients, including those with chronic kidney disease (CKD), who present with clinical, electrocardiogram (ECG), or imaging findings suspicious for acute myocardial infarction (AMI). Troponins are preferred to the MB isoenzyme of creatine kinase (CK-MB) because of their superior specificity and sensitivity for myocardial injury [1]. (See "Troponin testing: Clinical use".)

However, although still the preferred biomarker, troponins are more challenging to interpret for the diagnosis of AMI among CKD patients, compared with the general population. This is because stably elevated troponin concentrations are commonly observed in CKD patients in the absence of clinical evidence of myocardial damage [2-9]. In a systematic review and meta-analysis that included six studies of cTnT and eight studies of cTnI, the sensitivity and specificity for the diagnosis of acute coronary syndrome (ie, myocardial ischemia) ranged from 71 to 100 percent and 31 to 86 percent, respectively, for cTnT, and from 43 to 94 percent and 48 to 100 percent, respectively, for cTnI [10]. Only one study directly compared cTnT and cTnI in this review.

However, confidence in the results of this systematic review is limited. While the review is contemporary, many of the studies evaluated are not. Many of the reported assays have now been replaced by more sensitive versions (if not a high-sensitive version). Furthermore, the studies were extremely heterogeneous and used different assays and often different criteria for diagnosis. Several of the studies were originally designed to evaluate the prognostic value of troponins and thus used only a single value of troponin. Many studies relied on CK-MB for the diagnosis of MI. Neither use of a single troponin value nor use of CK-MB is consistent with the standard for diagnosis of MI reported by the Third Universal Definition of MI [1].

Specificity is even lower if newer, highly sensitive troponin assays are used [11,12]. (See "Troponin testing: Analytical aspects", section on 'Sensitive compared to highly sensitive assays'.) As an example, in one study that utilized a highly sensitive assay, among 122 patients with CKD (defined as estimated glomerular filtration rate [eGFR] <60 mL/min/1.73 m2) who presented with acute chest pain or dyspnea, the specificity of a single, elevated troponin on admission for AMI was 0.31, and the area under the curve for receiver operating characteristic (ROC) was only 0.54 [11]. The use of highly sensitive troponin assays is discussed elsewhere. (See "Troponin testing: Analytical aspects", section on 'Sensitive compared to highly sensitive assays'.)

The diagnostic accuracy of both high sensitive and sensitive (the clinically available assays in the United States) for the diagnosis of AMI was addressed in a prospective, observation study [9]. This multicenter, European-based study included 2813 subjects being evaluated for AMI, of whom 447 (16 percent) had renal dysfunction at the time of presentation. Renal dysfunction was defined as an eGFR of <60 mL/min/1.73 m2 calculated by the Modification of Diet in Renal Disease Study equation. Independent adjudicators confirmed a diagnosis of AMI using a high-sensitive troponin assay in 36 percent of those with renal dysfunction and 18 percent with normal renal function.

Based on the initial level of troponin, the overall accuracy for the diagnosis of AMI was acceptable for both sensitive and high-sensitive assays, although, depending on the assay, accuracy was lower for patients with renal dysfunction compared with those without. The differences in area under the curve for accuracy were most notable for the high-sensitive assays. However, the evaluation of serial samples over several hours, consistent with the universal definition of MI, resulted in an improvement in accuracy for AMI. This study highlights the challenges of using a 99th percentile value that is derived from a healthy general population to define a diagnostic threshold for AMI among patients with renal dysfunction. In contrast to patients with normal renal function, the majority of patients with renal dysfunction who are undergoing evaluation and do not have an AMI have a presenting troponin value above the 99th percentile value, particularly when measured with a high-sensitive assay.

The cause of low-level troponin elevations in CKD patients is likely chronic myocardial injury or underlying structural heart disease. Stably elevated troponin concentrations have been associated with a poor long-term survival among CKD patients. (See 'Use of troponins in prognosis' below.)

Despite the increased difficulty in interpretation compared with the general population, consensus guidelines recommend the use of troponins for AMI diagnosis among CKD patients because, as noted above, troponins are superior to CK-MB among CKD patients and in the general population [7]. (See "Criteria for the diagnosis of acute myocardial infarction", section on 'Cardiac biomarkers'.)

Among CKD patients who present with signs and symptoms suspicious for AMI, a change in troponin concentration (ie, rise or fall over three to six hours after presentation) should be used to define AMI, rather than a single value obtained on presentation [13]. The use of a dynamic change in troponin rather than a single value is consistent with the criteria for AMI for all patients (and not just CKD patients) established by the Joint Task Force of the European Society of Cardiology, American College of Cardiology Foundation, the American Heart Association, and the World Heart Federation (ESC/ACCF/AHA/WHF) [1]. (See "Criteria for the diagnosis of acute myocardial infarction", section on 'Third universal definition of MI'.)

We believe that either cTnT or cTnI may be used, providing serial concentrations are followed rather than single values and providing that the appropriate clinical context is present. Some clinicians prefer to use cTnI for the diagnosis of AMI among CKD patients. This is because of the belief that, compared with cTnT, cTnI is more specific for myocardial injury in CKD patients. This belief arose from the observation that, compared with cTnT, stably increased cTnI was less prevalent in CKD patients [4-6,14-18].

However, the detection of cTnI in asymptomatic CKD patients has become more common with the use of more sensitive generations of the cTnI assay, although cTnI is still detected less frequently than cTnT [19,20]. Consensus guidelines do not specify a preference for cTnI over cTnT for CKD patients [1,13]. If cTnI is used, one should not assume that a single increased value of cTnI (in absence of a dynamic change) is more diagnostic than that of cTnT.

The degree of elevation of either cTnT or cTnI that is required for the diagnosis of AMI among CKD patients is not known. The Third Universal Definition of MI specifies that, to meet the biomarker criteria for AMI, at least one troponin value should be above the 99th percentile upper reference limit provided by the manufacturer [1]. (See "Criteria for the diagnosis of acute myocardial infarction", section on 'Third universal definition of MI'.) However, as noted above, cardiac troponin values are commonly above the upper reference limit in CKD patients in the absence of AMI.

For CKD patients in whom all troponin levels are at or above the 99th percentile, a greater than 20 percent change in serially measured troponins is probably an acceptable threshold change for a positive AMI diagnosis, although there are no data available to support this approach. In addition, requiring such a serial change in this setting may lead to erroneously failing to diagnose AMI in some patients [21].

Some studies have attempted to define the optimal upper-limit threshold specifically for CKD patients. In one study of 75 patients with eGFR <60 mL/min/1.73 m2, an initial high cTnT (assayed with a highly sensitive test) was an accurate predictor of AMI (area under the curve for ROC of 0.96) when investigators used an upper-limit threshold that was more than twofold higher than the 99th percentile established by the manufacturer (36 ng/L compared with 14 ng/L) [12]. This higher cutoff resulted in sensitivity of 94 percent and specificity of 86 percent versus the lower cutoff (which had sensitivity of 100 percent and specificity of 54 percent) [12]. However, increasing the upper-limit threshold for AMI diagnosis may result in an unacceptable loss of sensitivity. We recommend using the 99th percentile value provided by the cardiac troponin assay manufacturer or local institution as the upper-limit threshold, rather than an alternative higher cutoff, to rule out or rule in an AMI.

The diagnostic accuracy of the high-sensitive assay may be decreased among dialysis patients since almost all patients have a baseline value above the 99th percentile. In one series of 670 consecutive dialysis patients who presented with chest pain or dyspnea, the area under the curve for ROC based on the initial high-sensitive cTnT was only 0.68 but improved to 0.9 with the addition of evaluation of relative change at three hours [22]. The optimal cut-off value was 24 percent.

Clinical judgment remains a critical component for the diagnosis of AMI among CKD patients. While using a dynamic change in troponin values improves the specificity for a diagnosis of AMI among CKD patients, exclusive reliance on such a change in addition to an elevated value could be associated with missing as many as 12 percent of non-ST elevation AMIs [23].

MB isoenzyme of creatine kinase fraction — When cardiac troponin is available, the CK-MB should not be used for the diagnosis of AMI. If CK-MB is the only assay available, it can be used, but it is far less sensitive and specific than troponins. Approximately 30 to 50 percent of dialysis patients without evidence of myocardial injury exhibit an elevation in the CK-MB fraction (defined as greater than 5 percent) [5,14,24,25].

The diagnosis of AMI should not be excluded based on the presence of CK-MB levels in the normal range and an elevated cardiac troponin level, due to the lower sensitivity of CK-MB. Likewise, the presence of an elevated CK-MB in the absence of an elevated cardiac troponin level needs further confirmation for a diagnosis of AMI due to the lack of specificity of CK-MB in patients with CKD.

USE OF TROPONINS IN PROGNOSIS — Increased troponins are associated with increased risk of short-term adverse cardiac outcomes among chronic kidney disease (CKD) patients diagnosed with acute myocardial infarction (AMI) [10,26-39].

A meta-analysis of three studies showed that the risk of cardiac mortality, AMI, ischemia, revascularization, dysrhythmia, congestive heart failure, and a composite of these outcomes increased with elevated cardiac troponin T (cTnT) [10]. Low-quality evidence suggested an increase in short-term overall mortality associated with cTnT in two studies. Elevated cardiac troponin I (cTnI) was associated with higher risk of short-term cardiac outcomes among dialysis patients in three studies.

Stably increased serum troponin levels also predict worse long-term cardiovascular outcomes and poor survival in asymptomatic CKD patients in the absence of AMI [27-38].

Among dialysis patients, the best data are from a 2014 systematic review with meta-analyses [39]. In a meta-analysis of pooled data from 11 studies adjusted for age and coronary artery disease (CAD) or CAD risk equivalent, elevated cTnT was associated with a threefold increase in all-cause mortality (95% CI 2.4-4.3) [39]. In a meta-analysis of seven studies that were similarly adjusted, cTnI was associated with a 2.7-fold increase in all-cause mortality (95% CI 1.9-4.6).

There were few studies utilizing the high-sensitive assay in this systematic review. However, cTnT measured using the high-sensitive assay has also been shown to be an independent predictor of all-cause mortality among dialysis patients [40,41].

Increased cardiac troponin levels have also been associated with poor outcomes among nondialysis CKD patients, although data are more limited. In the Trial to Reduce cardiovascular Events with Aranesp Therapy (TREAT), the first 1000 nondialysis CKD patients underwent measurement of cTnT using a contemporary (but non-high-sensitive) assay [42]. There was a correlation between detectable cTnT (≥0.01 ng/mL [≥10 ng/L], present in 45 percent) and cardiovascular events during the median follow-up period of 42.5 months. In a meta-analysis of two adequately adjusted studies, increased cTnT was associated with increased all-cause mortality, with pooled hazard ratio (HR) 3.4 (95% CI 1.1-11), but there was significant heterogeneity between studies [39]. A meta-analysis of two studies showed an association between increased cTnI and all-cause mortality (pooled HR 1.7, 95% CI 1.2-2.7) with no heterogeneity.

The prognostic utility of the high-sensitive assay has been evaluated among CKD patients. One small, multicenter study found that stably increased cTnT and cTnI, determined by high-sensitive assay, was associated with increased all-cause mortality among nondialysis CKD patients with estimated glomerular filtration rate (eGFR) <60 mL/min/1.73 m2 [19]. However, the association was attenuated when adjusted for renal function. Among 2464 individuals identified from the Chronic Renal Insufficiency Cohort (CRIC), increased cardiac troponin, measured using a high-sensitive assay, was detected in 81 percent of subjects and associated with worse renal function, traditional cardiovascular risk factors, black race, and increased left ventricular mass [43]. The outcomes associated with these higher levels in this cohort have yet to be published.

Cardiac troponins, particularly cTnT, have been used in some transplant centers to determine candidacy for kidney transplantation [37,44]. This issue is discussed elsewhere. (See "Evaluation of the potential renal transplant recipient", section on 'Cardiovascular disease'.)

EFFECT OF HEMODIALYSIS ON CARDIAC ENZYMES — Hemodialysis may change the concentration of cardiac enzymes. Concentrations could potentially increase due to hemo concentration or decrease due to clearance or binding to dialysis membrane of cardiac troponin fragments. Studies have yielded different results:

In one study, dialysis was shown to minimally change MB isoenzyme of creatine kinase (CK-MB) levels and not change cardiac troponin I (cTnI) levels [45].

Another study showed a decrease in both cTnI and cardiac troponin T (cTnT) levels (27 to 37 percent decrease, respectively) following dialysis with a high-flux membrane, but not with a low-flux membrane [46].

A third study found that cTnT concentrations were more likely to rise after dialysis in patients with known cardiovascular disease compared with those without known disease, suggesting that the rise in cTnT may be a result of cardiac injury [47].

The timing of hemodialysis should be considered when interpreting serial levels for acute myocardial infarction (AMI) diagnosis among hemodialysis patients. However, we believe that the criteria for a diagnosis of AMI should be the same for dialysis patients as for nondialysis chronic kidney disease (CKD) patients.

SUMMARY AND RECOMMENDATIONS

Cardiac troponins I and T (cTnI and cTnT) are the preferred biomarkers for the diagnosis of myocardial injury for patients with chronic kidney disease (CKD) who present with clinical, electrocardiogram (ECG), or imaging findings suspicious for acute myocardial infarction (AMI). Troponins are preferred to the MB isoenzyme of creatine kinase (CK-MB) because of their superior specificity and sensitivity for myocardial injury. (See "Troponin testing: Clinical use" and 'Troponins' above.)

A serial change (either a rise or fall) in troponin concentrations over three to six hours after presentation should be used to define AMI, rather than a single value obtained on presentation. This is because elevated troponin levels are commonly observed among CKD patients; thus, it is an increase in troponin levels, rather than a single elevated level at presentation, that should be used for diagnosis in the appropriate clinical setting. The use of a dynamic change in troponin rather than a single value is consistent with the criteria for AMI for all patients (and not just CKD patients) established by the Joint Task Force of the European Society of Cardiology, American College of Cardiology Foundation, the American Heart Association, and the World Heart Federation (ESC/ACCF/AHA/WHF). (See 'Troponins' above and "Criteria for the diagnosis of acute myocardial infarction", section on 'Third universal definition of MI'.)

Whether troponin-based criteria for diagnosis of AMI should be different in patients with CKD compared with those without CKD is not known. We recommend using the 99th percentile value provided by the cardiac troponin assay manufacturer or local institution as the upper limit of normal. Among patients in whom all troponin levels are at or above the 99th percentile, a greater than 20 percent change in serially measured troponins is probably an acceptable threshold change for a positive AMI diagnosis among CKD patients, although there are no data available to support this approach. In addition, requiring such a serial change in this setting may lead to failing to diagnose AMI in some patients. (See 'Troponins' above.)

Either cTnT or cTnI may be used for the diagnosis of AMI, providing serial concentrations rather than single values are followed and providing that the appropriate clinical context is present. Some clinicians prefer to use cTnI for the diagnosis of AMI among CKD patients because early troponin assays suggested that, compared with cTnT, cTnI was more specific for myocardial injury in CKD patients. However, increased cTnI levels are commonly detected in asymptomatic CKD patients when later, more sensitive generations of the cTnI assay are used. Consensus guidelines do not specify a preference for cTnI over cTnT for CKD patients. If cTnI is used, one should not assume that an increased single value of cTnI (in the absence of a dynamic change) is more diagnostic than that of cTnT. (See 'Troponins' above.)

When cardiac troponin is available, CK-MB should not be used for the diagnosis of AMI. If CK-MB is the only assay available, it can be used, but it is less sensitive and specific for AMI. The diagnosis of AMI should not be excluded based on the presence of CK-MB levels in the normal range if the cardiac troponin level is elevated due to the lower sensitivity of CK-MB. Likewise, the presence of an elevated CK-MB in the absence of an elevated cardiac troponin level needs further confirmation for a diagnosis of AMI due to the lack of specificity of CK-MB in CKD patients. (See 'MB isoenzyme of creatine kinase fraction' above.)

As for the general population, an increased troponin level is an independent prognosticator after the diagnosis of AMI. (See 'Use of troponins in prognosis' above.)

Increased troponin levels in stable, asymptomatic CKD patients predict worse long-term cardiovascular outcomes and poor survival. (See 'Use of troponins in prognosis' above.)

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