From the Guidelines
Elevated troponin levels in patients with chronic kidney disease (CKD) should be interpreted with caution, as they may not always indicate acute cardiac injury, and a threshold of <5 ng/L may rule out myocardial injury in this population. In CKD patients, baseline troponin levels are often chronically elevated due to decreased renal clearance, uremic myocardial damage, and underlying cardiovascular disease 1. When evaluating elevated troponin in CKD, clinicians should compare the current value to the patient's baseline if available, look for a rising or falling pattern (which suggests acute injury), and correlate with clinical symptoms and ECG changes. A single elevated troponin value in a CKD patient without symptoms or ECG changes may represent their chronic state rather than acute myocardial infarction.
Some key points to consider when interpreting elevated troponin in CKD patients include:
- The degree of elevation matters - very high levels or significant changes from baseline are more concerning for acute cardiac events
- CKD patients often have underlying cardiovascular disease, left ventricular hypertrophy, and microvascular damage that can cause ongoing minor troponin release
- High-sensitivity cardiac troponin (hs-cTn) assays maintain high diagnostic and prognostic accuracy and clinical utility in patients with renal dysfunction 1
- Patients with troponin concentrations >99th percentile have a two-fold greater risk of cardiac events at 1 year, irrespective of the diagnosis
The diagnosis of non-ST-segment elevation acute coronary syndromes (NSTE-ACS) in patients with CKD may be challenging, and new ECG changes should be differentiated from pre-existing abnormalities, and absolute changes in cardiac troponin should be assessed to differentiate MI from conditions associated with chronic cardiac injury 1. Despite these challenges, troponin remains useful in CKD patients when interpreted in the proper clinical context.
From the Research
Elevated Troponin in CKD
Elevated troponin levels in patients with chronic kidney disease (CKD) can be challenging to interpret, as these patients often have elevated troponin levels at baseline 2, 3, 4, 5, 6.
- The elevation of troponin T and troponin I in CKD patients is strongly correlated with adverse cardiovascular and all-cause mortality 2.
- The degree of troponin elevation appears to be predictive of the rate of renal decline via unclear mechanisms, though activation of the renin-angiotensin and other hormonal/oxidative stress systems remain suspect 2.
- In asymptomatic patients with CKD, research has shown increased prevalence of cardiovascular risk factors and underlying structural heart disease with increasing troponin levels 3.
- Prognostically, elevated troponin has been associated with adverse outcomes including incident heart failure and cardiovascular mortality 3, 4, 5.
Diagnostic Challenges
The diagnosis of acute myocardial infarction (AMI) in CKD patients is challenging due to their elevated troponin levels at baseline 2, 3, 4, 5, 6.
- The sensitivity of high-sensitivity cardiac troponins is preserved in the CKD population, but the specificity of these tests is compromised 2.
- The use of high-sensitivity troponin assays requires a nuanced approach, as the sensitivity and specificity for troponin testing in CKD varies 5.
- Concern for AMI with elevated troponin warrants treatment for AMI until proven otherwise, with consideration of atypical presentations along with other causes for patient symptoms that may result in troponin elevation 5.
Mechanisms of Troponin Elevation
The underlying etiology of persistently elevated troponin in the CKD population remains unclear, but several mechanisms have been proposed, including: