Elevated Troponin

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We had a lol come in yesterday (I had her last week too). She receives dialysis and has ESRD, DM, HTN, not sure what else. Anyway, she only has one arm to draw labs from and of course no one, not even VAT could access it. The doctor had to do an art stick and we got the blood from that. She originally came in for hypotension after 3 hours into dialysis. She was in the 80's systolic. My question is, her troponin and the rest of the cardiac markers were high this week and last week too but she had a normal EKG, would the abnormal cardiac markers be from the decreased cardiac output due to hypotension from dialysis or just the progression of her poor health? Neither the ED doctor and her nephrologist didn't seem too concerned about it there was no treatment initiated other than an abx for a uti.

I guess another question too is other than cardiac injuries what else can create abnormal cardiac markers? Thanks for your help!!!

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Ckd causes a strain on the heart so many of these pt have chronically elevated trops. My docs look at their baseline and as long as it is not an increase they aren't concerned. It's not an acute change and an expected part of the patho so usually not a worry.

Specializes in MICU.

The way I undrstand this is that, there is troponin in the skeletal muscle of the kidney. When there is injury to the kidney, the skeletal muscle breaks down and secrete troponin. So in this case, the elevated troponin is expected because the patient is ESRD. If you look at some of your patients chart, you will see that most of the time, there is always elevated troponin in ESRD, AKI, ARF &CKD. However, it is possible to have those disease and still have MI. You just have to look at the whole picture.

Specializes in Family Nurse Practitioner.

Any fluid overload which cause strech of (heart) muscles may cause a chronically high troponin. Dialysis and CHF patients can be effected.

Specializes in Cardiac, ER.
CAUSES — Troponin elevations have been reported in a variety of clinical scenarios other than an acute thrombotic occlusion of the coronary artery. One approach to describing these potential causes is to consider three major categories: 1) Myocardial damage related to secondary myocardial ischemia; 2) Myocardial damage related to non-ischemic causes; 3) Myocardial injury that is multifactorial or of indeterminate cause [8].

Below is a list of some of the causes for the elevation of troponin in the absence of an acute coronary syndrome, each of which can be grouped according to the three categories above (table 1) [2,8]. Notably, in some circumstances these potential categories of causes may be overlapping or impossible to discriminate completely from each other, such as in the case of patients with stable ischemic heart disease who become severely ill, tachycardic, and hypotensive with sepsis, or patients with severe heart failure and significantly elevated left ventricular end-diastolic pressure.

●Tachy- or bradyarrhythmias, or heart block

●Critically ill patients, especially with diabetes, respiratory failure or sepsis

●Hypertrophic cardiomyopathy

●Coronary vasospasm

●Acute neurological disease, including stroke or subarachnoid hemorrhage

●Cardiac contusion or other trauma including surgery, ablation, pacing, implantable cardioverter-defibrillator shocks, cardioversion, endomyocardial biopsy, cardiac surgery, following interventional closure of atrial septal defects.

●Rhabdomyolysis with cardiac injury

●Congestive heart failure (acute and chronic)

●Pulmonary embolism, severe pulmonary hypertension

●Renal failure

●Aortic dissection

●Aortic valve disease

●Apical ballooning syndrome - Takotsubo Cardiomyopathy

●Infiltrative diseases (ie, amyloidosis, hemochromatosis, sarcoidosis, and scleroderma)

●Inflammatory diseases (ie, myocarditis or myocardial extension of endo-/pericarditis, Kawasaki disease)

●Drug toxicity or toxins (ie, adriamycin, 5-flurouracil, herceptin, snake venom)

●Burns, especially if affecting >25 percent of body surface area

●Exertion

●Transplant vasculopathy

The 2012 joint European Society of Cardiology/American College of Cardiology/American Heart Association/World Health Federation(ESC/ACCF/AHA/WHF) task force recommends that an elevated value of cardiac troponin, in the absence of clinical evidence of ischemia, should prompt a search for other causes of myocardial necrosis as listed above [1,2]. We find it useful to consider whether the most likely cause is an acute cardiopulmonary condition, (such as myocarditis, pulmonary embolism, or heart failure), or a non-cardiopulmonary cause (such as sepsis or renal failure), as this consideration may be useful in directing the initial diagnostic evaluation.

In one series of 21 patients with elevated troponin levels and a normal coronary angiogram, the following etiologies for troponin elevations were suggested [9]:

●Tachycardia - 28 percent

●Pericarditis - 10 percent

●Heart failure - 5 percent

●Strenuous exercise - 10 percent

●No clear precipitating event - 47 percent

Elevated cardiac troponin concentration in the absence of an acute coronary syndrome

Specializes in Research & Critical Care.

Use of Cardiac Biomarkers in End-Stage Renal Disease

Differential diagnosis of elevated troponins

For answers to some of the whys you were asking

Thank you so much for all of your input. This definitely helps explain it further for me.

The way I undrstand this is that, there is troponin in the skeletal muscle of the kidney.

While its true that elevated troponin is common in patients with CKD, there is no kidney skeletal muscle.

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