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Cardiac troponin T in patients with kidney disease
1Clinical Department of Internal Medicine, Department of Nephrology, Teaching Hospital Maribor, Maribor, Slovenia. radovan.hojs@sb-mb.si
Insights
Dialysis patients have accelerated atherosclerosis and higher cardiovascular mortality. This review explores elevated cardiac troponin T (cTnT) in renal failure, suggesting subclinical myocardial issues rather than clearance problems.
Area of Science:
- Nephrology
- Cardiology
- Biochemistry
Background:
- Dialysis patients exhibit accelerated atherosclerosis and significantly higher cardiovascular mortality rates compared to the general population.
- Cardiac troponin T (cTnT) is a highly sensitive biomarker for myocardial necrosis, surpassing traditional cardiac enzymes in diagnostic utility.
Purpose of the Study:
- To review the significance of elevated cardiac troponin T (cTnT) in patients with varying degrees of renal failure and different treatment modalities.
- To explore potential causes of elevated cTnT in end-stage renal disease (ESRD) patients without acute coronary events.
Main Methods:
- Literature review of studies examining cardiac troponin T levels in patients with renal failure.
- Analysis of potential mechanisms for elevated cTnT, including decreased clearance, analytical interference, subclinical myocardial ischemia, and cardiac remodeling.
Main Results:
- Elevated cTnT is frequently observed in patients with renal failure, irrespective of treatment modality, even without acute coronary events.
- Decreased clearance or analytical interference from uremic serum are considered unlikely explanations for elevated cTnT.
- Elevated cTnT in ESRD patients is accepted as originating from myocytes, potentially due to subclinical myocardial ischemia, remodeling, or inflammation (uremic pericarditis/myocarditis).
Conclusions:
- Elevated cardiac troponin T in dialysis patients warrants further investigation into underlying cardiac pathology.
- The presence of elevated cTnT in renal failure may indicate subclinical myocardial damage or remodeling, contributing to increased cardiovascular risk.
Abstract:
Atherosclerosis is accelerated in dialysis patients and cardiovascular mortality is up to 20 times higher than in the general population. Cardiac troponin T (cTnT) is a sensitive marker of myocardial necrosis and studies have confirmed the superiority of this marker over traditional cardiac enzymes. Elevated cTnT has been observed in patients with various degrees of renal failure and treatment modalities in the absence of an acute coronary event. The possibility that increased troponins reflect decreased clearance or analytical interference from uremic serum is unlikely. It is accepted that cTnT detected in serum from patients with end-stage renal failure is derived from myocytes and this effect could be caused by subclinical myocardial ischemic release of troponin, myocardial remodeling, or from uremic pericarditis or myocarditis. The significance of cTnT in patients with different degrees of renal failure and different treatment modalities is presented in this review.
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