Why the study?
What is the clinical significance and etiology of elevated cardiac troponin T in patients with kidney disease?
What is the clinical significance and etiology of elevated cardiac troponin T in patients with kidney disease?
Elevated cardiac troponin T in patients with renal failure reflects true myocardial injury or remodeling rather than decreased clearance or assay interference.
Supports myocardial origin of cTnT elevation in ESRD; leaves open prospective validation before changing diagnostic thresholds.
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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Radovan Hojs (2005) studied this question.
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