Troponins, Acute Coronary Syndrome and Renal Disease: From Acute Kidney Injury Through End-stage Kidney Disease

Abstract

The diagnosis of acute coronary syndromes (ACS) is heavily dependent on cardiac biomarker assays, particularly cardiac troponins. ACS, particularly non-ST segment elevation MI, are more common in patients with acute kidney injury, chronic kidney disease (CKD) and end-stage kidney disease (ESKD), are associated with worse outcomes than in patients without kidney disease and are often difficult to diagnose and treat. Hence, early accurate diagnosis of ACS in kidney disease patients is important using easily available tools, such as cardiac troponins. However, the diagnostic reliability of cardiac troponins has been suboptimal in patients with kidney disease due to possible decreased clearance of troponin with acute and chronic kidney impairment and low levels of troponin secretion due to concomitant cardiac muscle injury related to left ventricular hypertrophy, inflammation and fibrosis. This article reviews the metabolism and utility of cardiac biomarkers in patients with acute and chronic kidney diseases. Cardiac troponins are small peptides that accumulate in both acute and chronic kidney diseases due to impaired excretion. Hence, troponin concentrations rise and fall with acute kidney injury and its recovery, limiting their use in the diagnosis of ACS. Troponin concentrations are chronically elevated in CKD and ESKD, are associated with poor prognosis and decrease the sensitivity and specificity for diagnosis of ACS. Yet, the evidence indicates that the use of high-sensitivity troponins can confirm or exclude a diagnosis of ACS in the emergency room in a significant proportion of kidney disease patients; those patients in whom the results are equivocal may need longer in-hospital assessment.

A 15-year-old with chest pain: An unexpected etiology

“…15 Another cause of elevated troponin-T includes kidney failure with increased creatinine, but our patient was found to have a normal creatinine, making this less likely. 16 Finally, troponin can be elevated following preload-induced mechanical stretch or physiologic stretches in otherwise normal hearts. 14 Given the fluid overload in our patient, myocardial strain caused by preload-induced wall stress was determined to be the etiology of the elevated troponin, especially in the setting of hypertensive emergency, which can exacerbate myocardial strain.…”

Male carriers of HLA-C*04:01 have increased risk of cardiac injury in COVID-19

“…In that regard, Dietl et al showed the convergence of hs-TnT in men and women post menopause with increasing age [19] . Subramanya et al demonstrated an increase in the left ventricular mass (LVM) as a result of an increasing androgen effect in postmenopausal women [20] . These findings provide a biologically plausible explanation for the increase in cardiac markers in men with COVID-19.…”

The LIFT trial: study protocol for a double-blind, randomised, placebo-controlled trial of K+-binder Lokelma for maximisation of RAAS inhibition in CKD patients with heart failure

“…Our hypothesis is that SZC therapy will reduce the incidence of treatment-limiting hyperkalaemia in CKD-HF patients, allowing higher doses of RAASi therapy and therefore better clinical outcomes. Achievement of the participant’s target RAASi dose is the primary endpoint, and secondary endpoints include measures to assess safety in terms of hyperkalaemia, cardiovascular risk in terms of troponin T levels [ 19 , 20 ], and efficacy in terms of time-to-target dose. We will also assess the impact of achieving target RAASi dosing on hospital admission rates and duration of stay, with the hope that optimum RAASi treatment will translate into reduced morbidity and improved QoL.…”