Troponin I levels in a hemolytic uremic syndrome patient with severe cardiac failure

Abstract

Troponins are highly sensitive and specific biochemical markers of myocardial injury that are released into the circulation during myocardial ischemia. We describe changes in cardiac troponin I (cTnI) prior to and following clinical evidence of severe myocardial dysfunction in a child with hemolytic uremic syndrome (HUS). A previously healthy, 22-month-old girl presented with typical HUS and stool cultures positive for Escherichia coli O157:H7. She required dialysis, blood and platelet transfusions, and insulin for HUS-related diabetes mellitus. On the 6th hospital day she had sudden circulatory collapse with a blood pressure of 70/40 mmHg and an oxygen saturation of 88%. She responded rapidly to emergency resuscitation but had diminished left ventricular function (ejection fraction 18%). Four days after the acute event an echocardiogram showed normal ventricular size and contractility. She underwent hemodialysis for 22 days, and renal function was normal after 33 days. cTnI levels were measured with a microparticle enzyme immunoassay. cTnI was normal (>0.4 microg/l) 32 h prior to cardiac collapse, mildly increased (2.1 microg/l) 8 h before the cardiac collapse, severely elevated shortly after the cardiac event (43.1 microg/l), and peaked (140.6 microg/l) at 24 h. It then fell gradually and was normal at discharge. These results suggest that measurement of cTnI may be a useful predictor of cardiac involvement in severely affected children with HUS.

Treatment and outcome of Shiga-toxin-associated hemolytic uremic syndrome (HUS)

“…Central nervous system (CNS) involvement in typical HUS is common and frequently presents as lethargy, irritability, and seizures, and in more severe cases, CNS disease presents as paresis, coma, and cerebral edema. Skeletal muscle involvement manifested as rhabdomyolysis occurs in rare cases, and fortunately, myocardial involvement is rare as well [80, 81]. When myocardial involvement occurs, elevated troponin I level may reflect the degree of myocardial ischemia [81].…”

Case Report On Haemolytic Uraemic Syndrome And Cardiovascular Complication

“…6 Cardiovascular complications have been reported in children in the literature up to 10% of children with HUS during the 1993 epidemic of E-coli 0157:H7 in the Western USA and congestive cardiac failure is more common in adults with HUS. 7,8 The increase in the concentrations of troponin I during HUS in our case with clinical description of cardiac chest pain and radiological of pulmonary oedema should be attributed to cardiac ischaemia. 7,8 This patient has significantly raised troponin I and echocardiographic evidence of acute cardiac failure based on the Framingham Study Criteria (left ventricular ejection fraction ≤ 40% or an acute reduction ≥15%).…”

Cardiovascular impairment in Shiga-toxin-2-induced experimental hemolytic–uremic syndrome: a pilot study

“…The origin of the increase in cTnI in HUS remains unknown; however, thrombotic microangiopathy of cardiac vessels (see above) has been found in two autopsy studies of children who died from HUS ( 23 ). In a case report of cardiovascular impairment in HUS, the temporal dynamics of plasma troponin were recorded around the cardiac event, showing a peak troponin level 24 h after the event and mild elevations 8 h before the event ( 5 ). Should the mouse model prove consistent with this finding, the mild increase in cTnI levels seen in some mice could potentially be indicative of a future cardiac event rather than a past one (i.e., acute myocardial infarction).…”

“…Cardiac troponin I (cTNI), one of three isoforms, is a specific serum marker of cardiac injury. Increases of cTNI can occur prior to and following severe myocardial dysfunction in HUS ( 5 ); however, as troponins are excreted via the kidney, their concentrations may also increase during AKI in the absence of myocardial damage [reviewed in ( 7 )]. In some cases, the cause for the observed cardiac events during HUS was suspected to be ischemic in nature ( 8 ).…”