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Specificity of cardiac troponins I and T in renal disease
S Willging1, F Keller, G Steinbach
1Abteilung Innere Medizin II, Universitätsklinikum Ulm, Germany.
Insights
Cardiac troponin I (cTnI) is more specific than cardiac troponin T (cTnT) in hemodialysis patients. Uremic myopathy may cause falsely elevated cTnT levels in these patients, impacting cardiac biomarker accuracy.
Area of Science:
- Nephrology
- Cardiology
- Clinical Chemistry
Background:
- Cardiac troponins are critical biomarkers for myocardial infarction.
- Renal impairment can affect troponin levels, complicating diagnosis.
- Comparing cardiac troponin I (cTnI) and cardiac troponin T (cTnT) specificity in renal patients is essential.
Purpose of the Study:
- To compare the diagnostic specificity of serum cTnI and cTnT levels in renal patients.
- To evaluate the impact of different renal replacement therapies on troponin specificity.
- To investigate potential reasons for discordant troponin results in hemodialysis patients.
Main Methods:
- Serum cTnI and cTnT levels were measured in 85 renal patients (chronic renal impairment, peritoneal dialysis, hemodialysis).
- Exclusion criteria included acute cardiac events and conditions affecting muscle enzymes.
- Specificity was calculated, and correlations with dialysis duration were assessed.
Main Results:
- Cardiac troponin I demonstrated higher specificity across all renal patient groups compared to cTnT.
- cTnT specificity was significantly lower in long-term hemodialysis patients (46%) than in others.
- No significant difference in troponin levels pre- and post-hemodialysis explained the discordant results.
Conclusions:
- Cardiac troponin I offers superior specificity to cTnT in hemodialysis patients.
- Falsely elevated cTnT levels in hemodialysis patients may be attributed to uremic myopathy.
- cTnI is a more reliable biomarker for cardiac events in patients with end-stage renal disease.
Unlabelled:
We investigated and compared serum levels of cardiac troponins I(cTnl) and cardiac troponin T (cTnT) in 85 renal patients (chronic renal impairment n = 23, continuous ambulatory peritoneal dialysis n = 20, hemodialysis n = 42). Patients with the following conditions were excluded: myocardial infarction, angina pectoris, liver disease, malignant neoplasms, enforced physical activity, skeletal muscle trauma, myositis, rhabdomyolysis and seizures. Troponin T was measured by the second generation cTnT-ELISA with a cut-off value = 0.1 microgram/l. Troponin I was measured by a cTnI immunoassay analyser with a cut-off value = 2.0 micrograms/l. Additionally, creatine kinase (CK), CK-MB activity, CK-MB mass concentration and myoglobin levels were measured. Specificity was determined as the fraction of true-negative cases compared to the total number of false-positive and true-negative cases. Specificity for cTnT was 96% [78-100] in patients with renal impairment (creatinine > 150 mumol/l), 95% [75-100] in continuous ambulatory peritoneal dialysis patients, but in hemodialysis patients it was 75% [53-92] for short-term hemodialysis (< 1 year) and 46% [24-68] for long-term hemodialysis (> 1 year). There was a weak correlation between cTnT levels and duration of hemodialysis therapy (r = 0.35, n = 34, p < 0.04). Specificity for cTnI in renal impairment patients was 96% [78-100] and 100% [84-100] in continuous ambulatory peritoneal dialysis and all hemodialysis patients. None of the studied markers showed higher specificity than cTnI. Only myoglobin was less specific than cTnT in hemodialysis patients. Different clearances of the troponins during dialysis (investigated by pre-hemodialysis and post-hemodialysis levels) cannot explain the discordant results of cTnT and cTnI.
Conclusion:
Cardiac troponin I exhibits higher specificity than cardiac troponin T in hemodialysis patients. Uremic myopathy could explain falsely elevated troponin T levels in hemodialysis patients.