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Cardiac troponins in patients with kidney disease

Cardiac troponins in patients with kidney disease
Author:
Christopher deFilippi, MD, FACC
Section Editors:
Jeffrey S Berns, MD
Allan S Jaffe, MD
Nisha Bansal, MD
Deputy Editor:
Eric N Taylor, MD, MSc, FASN
Literature review current through: May 2024.
This topic last updated: Apr 24, 2024.

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

This topic reviews the clinical use of cardiac troponins in patients with CKD. The use of cardiac troponins in patients with normal kidney function is discussed separately. (See "Troponin testing: Clinical use".)

The use of liver and pancreatic enzymes in patients with CKD is discussed separately. (See "Serum enzymes in patients with kidney failure".)

The risk of coronary artery disease among patients with CKD, including those on dialysis, is presented elsewhere. (See "Chronic kidney disease and coronary heart disease" and "Clinical manifestations and diagnosis of coronary artery disease in end-stage kidney disease (dialysis)".)

INTERPRETING TROPONIN LEVELS IN PATIENTS WITH CKD

Effect of CKD on troponin levels — Cardiac troponin levels are challenging to interpret among patients with chronic kidney disease (CKD). This is due to the high prevalence of stably elevated troponin levels in the absence of clinical evidence of acute myocardial infarction (AMI) among patients with CKD [2-6].

The cause of low-level cardiac troponin elevations in patients with CKD is likely chronic myocardial injury that is not a result of epicardial coronary disease. Several lines of evidence support that increased cardiac release of troponins, rather than decreased kidney clearance, is the primary cause of elevated basal levels in patients with CKD [7]. (See 'Use of troponins in prognosis' below.)

With the transition to highly sensitive (hs) troponin assays throughout the world, the majority of patients with CKD will have measurable troponin levels. In the National Institutes of Health Chronic Renal Insufficiency Cohort (CRIC) study, 81 percent of over 2400 participants with CKD and measured hs cardiac troponin T (hs-cTnT) levels had a detectable level (>3 ng/L) [2]. Furthermore, many patients with CKD will have baseline hs troponin values that exceed the 99th percentile for healthy adults, a cutoff above which a patient is considered to have "myocardial injury" by the Fourth Universal Definition of Myocardial Infarction. In a study of patients presenting for the evaluation of possible AMI at two Scottish hospitals, the proportion of patients with CKD who had a hs cardiac troponin I (hs-cTnI) value above the 99th percentile increased with progressively impaired kidney function, with over 60 percent exceeding this threshold when the estimated glomerular filtration rate was <30 mL/min per 1.73 m2 [3]. In another study of over 2300 CRIC participants with CKD and no self-reported history of cardiovascular disease, the 99th percentile of hs-cTnT (126 ng/L) was substantially higher than the 99th percentile sex neutral value for this assay in the United States (19 ng/L), and each 15 mL/min/1.73m2 decrement in estimated glomerular filtration rate was associated with an approximately 40 percent higher threshold for the 99th percentile value of hs-cTnT [8].

Effect of dialysis on troponin levels — Hemodialysis may change the concentration of cardiac troponins. Levels of these biomarkers could potentially increase due to hemoconcentration or decrease due to clearance or binding to dialysis membrane of cardiac troponin fragments. Thus, differences may in part be related to the diffusion rates, dialysis gradient, and pore size of the dialysis membranes in use. Studies have yielded conflicting results:

●In one study, hemodialysis was shown to minimally change MB isoenzyme of creatine kinase (CK-MB) levels and not change cTnI levels [9].

●Another study showed a decrease in both cTnI and cTnT levels (27 to 37 percent decrease, respectively) following hemodialysis with a high-flux membrane but not with a low-flux membrane [10].

●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 [11].

Data on the effect of peritoneal dialysis on cardiac troponin levels are more limited. One study found lower cTnI levels among patients on peritoneal dialysis compared with those on hemodialysis [12].

Cardiac troponin levels may also be altered by continuous kidney replacement therapy (CKRT) when used as a therapy. As an example, a study of 10 critically ill patients with acute kidney injury requiring CKRT found a 52 percent decline in hs-cTnT in the first 5 to 10 hours, followed by a plateau for the duration of time on CKRT; serum albumin remained stable and creatinine declined over the entire course of treatment [13].

The timing of hemodialysis and CKRT should be considered when interpreting serial levels for AMI diagnosis among patients receiving such modalities. However, we believe that the criteria for a diagnosis of AMI should be the same for patients on dialysis as for patients with CKD who are not on dialysis. (See 'Evaluation of suspected myocardial infarction' below.)

EVALUATION OF SUSPECTED MYOCARDIAL INFARCTION — Cardiac troponins T and I (cTnT and cTnI) are the blood-based biomarkers that are used for the diagnosis of myocardial injury or infarction among patients who present with clinical, electrocardiogram, or imaging findings suspicious for acute myocardial infarction (AMI) [1]. Cardiac troponins are preferred to the MB isoenzyme of creatinine kinase (CK-MB) because of their superior specificity and sensitivity for myocardial injury. (See "Troponin testing: Clinical use".)

Interpreting cardiac troponin levels in the setting of chronic kidney disease (CKD) is challenging (see 'Interpreting troponin levels in patients with CKD' above). We take the following approach:

●No modification based on kidney function – The initial clinical protocols we use to evaluate suspected AMI in patients with CKD, regardless of stage, are the same as those we use for patients without CKD. These protocols incorporate the absolute value of and change in serial troponin measurements, typically obtained between one and three hours apart [14,15]. We do not modify upper-limit threshold troponin values for patients with CKD. (See "Diagnosis of acute myocardial infarction" and "Troponin testing: Clinical use".)

Our approach maintains a very high sensitivity for AMI diagnosis but results in a decreased specificity for patients with CKD, many of whom will fall into an indeterminate risk group and require a more extended cardiac evaluation [14,15]. This strategy is in agreement with contemporary expert Consensus Decision Pathways for the evaluation of suspected AMI, which do not provide different guidance for patients with CKD [14,15].

Using individualized baseline troponin values may facilitate the evaluation of suspected AMI among patients with CKD; however, this approach has not been evaluated in clinical trials.

●Choice of troponin – We believe that either cTnT or cTnI may be used, provided that serial concentrations are followed rather than single values and that the appropriate clinical context is present. Some clinicians prefer to use cTnI for the diagnosis of AMI among patients with CKD. This is because of the belief that, compared with cTnT, cTnI is more specific for myocardial injury in patients with CKD. This belief arose from the observation that, compared with cTnT, stably increased cTnI was less prevalent in patients with CKD [16-23].

However, the detection of cTnI in asymptomatic patients with CKD has become more common with the use of more sensitive generations of the cTnI assay [24,25]. Consensus guidelines do not specify a preference for cTnI over cTnT for patients with CKD [1,14,15,26]. Observational data in an emergency department population suggest that results are similar with a highly sensitive cTnI (hs-cTnI) and highly sensitive cTnT (hs-cTnT) with respect to both diagnosis and prognosis [4].

The diagnostic accuracy of hs-cTnI and hs-cTnT among patients with CKD presenting to emergency departments with suspected AMI has been evaluated in three prospective, observational studies [3-5]:

●In one study, an initially low hs-cTnI value of <5 ng/L at presentation had a similar negative predictive value (NPV) for the diagnosis of AMI among patients with and without CKD (98.4 versus 99.7 percent, respectively) [3]. The positive predictive value (PPV) of a hs-cTnI at the 99th percentile was lower for patients with CKD compared with those without CKD (50 versus 62 percent, respectively).

●Similar findings were reported in a second study that evaluated the diagnostic accuracy of baseline and serial hs-cTnI measurements for AMI among 1555 adults presenting to the emergency department with symptoms suggesting ischemia [5]. Kidney function impairment did not affect the NPV of serial hs-cTnI for diagnosing AMI; however, PPV decreased with worsening kidney function (51 to 57 percent with normal kidney function versus 27 to 42 percent with severely impaired kidney function [estimated glomerular filtration rate <30 mL/min per 1.73 m2] versus 15 to 32 percent on dialysis).

●An alternative approach to the evaluation of patients with CKD presenting for the evaluation of AMI is the clinical decision pathway (CDP), which involves measuring a troponin using a high-sensitivity assay at baseline and again at one to two hours [27]. The CDP triages patients in this time frame to "rule-out," "observation," and "rule-in" status. The efficacy of the pathway is determined by the percentage of patients who can be triaged to "rule-out" or "rule-in" and not "observation" status. In a multicenter European study of 3254 patients (15 percent with CKD), the efficacy of the CDP using hs-cTnT was 51 percent in patients with CKD, compared with 81 percent in those without CKD; similar findings were seen with a simultaneously measured hs-cTnI assay [4]. Optimization of hs-cTn "rule-in" and "rule-out" thresholds for patients with CKD did not improve efficacy of the CDP.

The diagnostic accuracy of the high-sensitivity assay may be further decreased among patients on dialysis since almost all patients have a baseline value above the 99th percentile established in a healthy general population. In one series of 670 consecutive patients on dialysis who presented with chest pain or dyspnea, the area under the curve for receiver operating characteristic to diagnose an AMI based on the initial hs-cTnT was only 0.68 but improved to 0.9 with the addition of evaluation of relative change of ≥24 percent at three hours [28].

Clinical judgment with a high index of suspicion remains a critical component for the diagnosis of AMI among patients with CKD. While using a dynamic change in troponin values improves the specificity for a diagnosis of AMI in this population, 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 in all patients irrespective of kidney function [29].

USE OF TROPONINS IN PROGNOSIS — Increased troponins are associated with increased risk of short-term adverse cardiac outcomes among patients with chronic kidney disease (CKD) who are diagnosed with acute myocardial infarction (AMI) [4,30-44]. As an example, a meta-analysis of three studies of patients with CKD and suspected acute coronary syndrome found that the risk of cardiac mortality, AMI, ischemia, revascularization, dysrhythmia, heart failure, and a composite of these outcomes increased with elevated cardiac troponin T (cTnT) [30]. Data from subsequent multicenter studies have also shown that levels of both high-sensitivity cardiac troponin I (cTnI) and high-sensitivity cTnT can effectively prognosticate patients with and without CKD [3,4].

Stably increased circulating cTnI and cTnT levels also predict worse long-term cardiovascular outcomes and poor survival in asymptomatic patients with CKD in the absence of AMI, whether or not they receive dialysis [39,44,45]. Higher values are associated with a worse prognosis.

The prognostic utility of the high-sensitivity assay has been evaluated among patients with CKD who are not on dialysis. Among 2464 individuals identified from the Chronic Renal Insufficiency Cohort (CRIC), increased cTnT, measured using a high-sensitivity assay, was detected in 81 percent of subjects; higher cardiac troponin was associated with worse kidney function, traditional cardiovascular risk factors, increased left ventricular mass, and increased incidence of heart failure [2,45].

Some transplant centers incorporate cardiac troponins, particularly cTnT, into their assessment of cardiac risk in potential kidney transplant recipients [42,46,47]. This issue is discussed elsewhere. (See "Kidney transplantation in adults: Evaluation of the potential kidney transplant recipient", section on 'Cardiovascular disease'.)

SUMMARY AND RECOMMENDATIONS

●Effect of chronic kidney disease on troponin levels – Cardiac troponin levels are challenging to interpret among patients with chronic kidney disease (CKD). This is due to the high prevalence of stably elevated troponin levels in the absence of clinical evidence of acute myocardial infarction (AMI) among patients with CKD. The cause of low-level cardiac troponin elevations in patients with CKD is likely chronic myocardial injury that is not a result of epicardial coronary disease. (See 'Effect of CKD on troponin levels' above.)

●Evaluation of suspected myocardial infarction – The initial clinical protocols we use to evaluate suspected AMI in patients with CKD, regardless of stage, are the same as those we use for patients without CKD. These protocols incorporate the absolute value of and change in serial troponin measurements, typically obtained between one and three hours apart. Our approach maintains a very high sensitivity for AMI diagnosis but results in a decreased specificity for patients with CKD, many of whom will fall into an indeterminate risk group and require a more extended cardiac evaluation. (See 'Evaluation of suspected myocardial infarction' above.)  

●Use of troponins in prognosis – Increased troponins are associated with increased risk of short-term adverse cardiac outcomes among patients with CKD who are diagnosed with AMI. Stably increased serum troponin levels also predict worse long-term cardiovascular outcomes and poor survival in asymptomatic patients with CKD in the absence of AMI, whether or not they receive dialysis. Higher values are associated with a worse prognosis. (See 'Use of troponins in prognosis' above.)

ACKNOWLEDGMENT — The UpToDate editorial staff acknowledges William Henrich, MD, MACP, who contributed to earlier versions of this topic review.

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Topic 1920 Version 26.0

References

1 : Fourth Universal Definition of Myocardial Infarction (2018).

2 : Predictors of high sensitivity cardiac troponin T in chronic kidney disease patients: a cross-sectional study in the chronic renal insufficiency cohort (CRIC).

3 : High-Sensitivity Cardiac Troponin and the Risk Stratification of Patients With Renal Impairment Presenting With Suspected Acute Coronary Syndrome.

4 : 0/1-Hour Triage Algorithm for Myocardial Infarction in Patients With Renal Dysfunction.

5 : Renal Dysfunction Influences the Diagnostic and Prognostic Performance of High-Sensitivity Cardiac Troponin I.

6 : Variation of NT-proBNP and High-Sensitivity Cardiac Troponin T Across Levels of Estimated Glomerular Filtration Rate: The SPRINT Trial.

7 : Cardiac Troponin T: Smaller Molecules in Patients with End-Stage Renal Disease than after Onset of Acute Myocardial Infarction.

8 : Upper Reference Limits for High-Sensitivity Cardiac Troponin T and N-Terminal Fragment of the Prohormone Brain Natriuretic Peptide in Patients With CKD.

9 : Specificity of cardiac troponin I and creatine kinase-MB isoenzyme in asymptomatic long-term hemodialysis patients and effect of hemodialysis on these cardiac markers.

10 : Influence of sampling time and ultrafiltration coefficient of the dialysis membrane on cardiac troponin I and T.

11 : Cardiac troponin T and I in end-stage renal failure.

12 : Plasma myeloperoxidase, NT-proBNP, and troponin-I in patients on CAPD compared with those on regular hemodialysis.

13 : Variation of High-Sensitivity Troponin T Results in Patients Undergoing Continuous Renal Replacement Therapy.

14 : 2022 ACC Expert Consensus Decision Pathway on the Evaluation and Disposition of Acute Chest Pain in the Emergency Department: A Report of the American College of Cardiology Solution Set Oversight Committee.

15 : 2020 ESC Guidelines for the management of acute coronary syndromes in patients presenting without persistent ST-segment elevation.

16 : Predictive value of cardiac troponin I and T for subsequent death in end-stage renal disease.

17 : Cardiac troponin I, cardiac troponin T, and creatine kinase MB in dialysis patients without ischemic heart disease: evidence of cardiac troponin T expression in skeletal muscle.

18 : Are cardiac troponins reliable serodiagnositic markers of cardiac ischaemia in end-stage renal disease?

19 : Cardiac troponin I. A marker with high specificity for cardiac injury.

20 : Cardiac troponins in serum in chronic renal failure.

21 : Cardiac troponin T is elevated in asymptomatic patients with chronic renal failure.

22 : Cardiac troponin I and creatine kinase-MB mass to rule out myocardial injury in hospitalized patients with renal insufficiency.

23 : Performance of multiple cardiac biomarkers measured in the emergency department in patients with chronic kidney disease and chest pain.

24 : Interpreting cardiac troponin results from high-sensitivity assays in chronic kidney disease without acute coronary syndrome.

25 : Cardiac troponin I concentration is commonly increased in nondialysis patients with CKD: experience with a sensitive assay.

26 : Recommendations for Institutions Transitioning to High-Sensitivity Troponin Testing: JACC Scientific Expert Panel.

27 : 2015 ESC Guidelines for the management of acute coronary syndromes in patients presenting without persistent ST-segment elevation: Task Force for the Management of Acute Coronary Syndromes in Patients Presenting without Persistent ST-Segment Elevation of the European Society of Cardiology (ESC).

28 : Diagnosis of Acute Myocardial Infarction in Hemodialysis Patients With High-Sensitivity Cardiac Troponin T Assay.

29 : Small changes in troponin T levels are common in patients with non-ST-segment elevation myocardial infarction and are linked to higher mortality.

30 : Role of troponin in patients with chronic kidney disease and suspected acute coronary syndrome: a systematic review.

31 : Troponin T levels in patients with acute coronary syndromes, with or without renal dysfunction.

32 : Cardiac troponin T predicts mortality in patients with end-stage renal disease.

33 : Prognostic value of troponin T in hemodialysis patients is independent of comorbidity.

34 : Cardiac troponin T and C-reactive protein for predicting prognosis, coronary atherosclerosis, and cardiomyopathy in patients undergoing long-term hemodialysis.

35 : Serum troponin T measurement in patients with chronic renal impairment predicts survival and vascular disease: a 2 year prospective study.

36 : Measurement of circulating troponin Ic enhances the prognostic value of C-reactive protein in haemodialysis patients.

37 : Prognostic value of cardiac markers in ESRD: Chronic Hemodialysis and New Cardiac Markers Evaluation (CHANCE) study.

38 : Use of cardiac troponin T in diagnosis and prognosis of cardiac events in patients on chronic haemodialysis.

39 : Prognostic value of troponin T and I among asymptomatic patients with end-stage renal disease: a meta-analysis.

40 : Serum troponin T concentration as a predictor of mortality in hemodialysis and peritoneal dialysis patients.

41 : Troponin T, left ventricular mass, and function are excellent predictors of cardiovascular congestion in peritoneal dialysis.

42 : Survival of patients on the kidney transplant wait list: relationship to cardiac troponin T.

43 : Cardiac troponin T predicts occult coronary artery stenosis in patients with chronic kidney disease at the start of renal replacement therapy.

44 : Prognostic value of cardiac troponin in patients with chronic kidney disease without suspected acute coronary syndrome: a systematic review and meta-analysis.

45 : High-sensitivity troponin T and N-terminal pro-B-type natriuretic peptide (NT-proBNP) and risk of incident heart failure in patients with CKD: the Chronic Renal Insufficiency Cohort (CRIC) Study.

46 : Cardiac disease evaluation and management among kidney and liver transplantation candidates: a scientific statement from the American Heart Association and the American College of Cardiology Foundation.

47 : Emerging Evidence on Coronary Heart Disease Screening in Kidney and Liver Transplantation Candidates: A Scientific Statement From the American Heart Association: Endorsed by the American Society of Transplantation.

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