Elevated Troponin in presence of Renal Failure

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Hi, I am working in a Critical Cardiac unit that also takes MICU patients as overflow. There have been a few times that I have found that my patient (who is in some phase of renal failure) has elevated troponin however show no signs of an MI. I have been told by a few nurses that in renal failure, troponins may be elevated due to the renal failure and not an MI. Can anyone confirm this, or more importantly explain why this occurs?

I'd think that it is simply troponins build up due to the decreased filtration. However I have not been able to find anything to back this up.

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Specializes in Nephrology, Cardiology, ER, ICU.

I took the following from UpToDate:

Troponins — Cardiac troponins T and I (cTnT and cTnI) are the preferred biomarkers for the diagnosis of myocardial injury for all patients, including those with chronic kidney disease (CKD), who present with clinical, electrocardiogram (ECG), or imaging findings suspicious for acute myocardial infarction (AMI). Troponins are preferred to the MB isoenzyme of creatine kinase (CK-MB) because of their superior specificity and sensitivity for myocardial injury [1].

However, although still the preferred biomarker, troponins are more challenging to interpret for the diagnosis of AMI among CKD patients, compared with the general population. This is because stably elevated troponin concentrations are commonly observed in CKD patients in the absence of clinical evidence of myocardial damage [2-8]. In a systematic review and meta-analysis that included six studies of cTnT and eight studies of cTnI, the sensitivity and specificity for the diagnosis of acute coronary syndrome (ie, myocardial ischemia) ranged from 71 to 100 percent and 31 to 86 percent, respectively, for cTnT, and from 43 to 94 percent and 48 to 100 percent, respectively, for cTnI [9]. Only one study directly compared cTnT and cTnI in this review.

However, confidence in the results of this systematic review is limited. While the review is contemporary, many of the studies evaluated are not. Many of the reported assays have now been replaced by more sensitive versions (if not a high-sensitive version). Furthermore, the studies were extremely heterogeneous and used different assays and often different criteria for diagnosis. Several of the studies were originally designed to evaluate the prognostic value of troponins and thus used only a single value of troponin. Many studies relied on CK-MB for the diagnosis of MI. Neither use of a single troponin value nor use of CK-MB is consistent with the standard for diagnosis of MI reported by the Third Universal Definition of MI [1].

Specificity is even lower if newer, highly sensitive troponin assays are used [10,11]. As an example, in one study that utilized a highly sensitive assay, among 122 patients with CKD (defined as estimated glomerular filtration rate [eGFR] 10]. The use of highly sensitive troponin assays is discussed elsewhere. (

The cause of low-level troponin elevations in CKD patients is likely chronic myocardial injury or underlying structural heart disease. Stably elevated troponin concentrations have been associated with a poor long-term survival among CKD patients.

I bolded the important part.

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Specializes in Dialysis.

Myocardial stunning also occurs during dialysis treatments due to the large volume changes that occur and the drop in blood pressure. 1/3 of all dialysis treatments will involve hypotension as fluid is removed from the blood it has to be replaced by fluid from the tissue. Leaky capillaries, low albumin and autonomic dysfunction also play a role. We try as dialysis nurses to minimize this pressure drop but when you remove 3-4 liters in 3-4 hours many patients do not tolerate this well. The cardiac damage is real, the answer is longer treatment times, and I have yet to meet the patient that wants longer treatment times.

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