How are troponins used as cardiac markers in chronic renal failure (CRF)?

Updated: Jul 30, 2021
  • Author: Kamal (Komo) Gursahani, MD, MBA; Chief Editor: Barry E Brenner, MD, PhD, FACEP  more...
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Patients with chronic renal failure (CRF) who are on hemodialysis are at increased risk of coronary artery disease and acute coronary syndrome (ACS), and cardiovascular disease accounts for about 50% of deaths in these patients. Early studies revealed a high prevalence of elevated cardiac troponin (cTn) levels in patients with CRF, especially troponin T (TnT). However, the clinical significance of an elevated TnT result is unclear.

Biochemical studies have demonstrated that the troponin elevation originates from the myocardium and is not related to the myopathy associated with renal failure. Yet, patients with CRF frequently have chronic congestive heart failure (CHF) and hypertension, which may independently elevate the troponin level. In addition, data suggest that elevated troponin levels in asymptomatic patients may reflect subclinical microinfarctions that are clinically distinct from ACS.

Large prospective studies have confirmed the association between TnT elevation and cardiac mortality in patients with CRF. The GUSTO IV ACS trial showed that patients with renal insufficiency and an elevated TnT had the highest overall risk of the composite endpoint of death or acute myocardial infarction (MI), [64] and two other prospective studies reported that an elevated TnT—but not troponin I (TnI)—increased the risk of long-term mortality. [65, 66] Whether elevated TnT increases cardiac risk in the short term (ie, 30 d) is unclear, but patients without short-term risk may not require hospitalization and potentially could be managed on an outpatient basis.

It has been suggested that chronically elevated troponin levels represent chronic structural cardiovascular disease, such as prior MI, chronic CHF, or hypertension in the setting of CRF. If true, these patients are at higher cardiac risk compared with the normal, healthy patient population, and troponin remains a useful marker in the setting of CRF. [67, 68]

Note that dialysis does not affect TnT or TnI levels; predialysis and postdialysis levels are essentially unchanged. Creatine kinase (CK)-MB, however, is dialyzable, and levels are decreased postdialysis. Therefore, a single elevated TnT level in patients with CRF and possible ACS is nondiagnostic for acute MI in the absence of other findings. Serial determinations are usually required, with a focus on a rise in the troponin level.

Ascertaining whether an elevated troponin in patients with CRF represents true acute MI or a false-positive result can be difficult. In patients with cardiac risk factors who are deemed clinically to be at moderate-high risk for ACS, the prudent approach would be to observe and perform serial cardiac markers over 6-9 hours. In low-risk asymptomatic patients and in the absence of any other findings indicative of ACS, the elevated troponin result is more likely to be false positive for acute MI.

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