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

Debasish Banerjee, Charlotte Perrett, Anita Banerjee, Debasish Banerjee, Charlotte Perrett, Anita Banerjee

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.

Keywords: Acute kidney injury; acute coronary syndrome; cardiac troponin; chronic kidney disease; end-stage kidney disease; non-ST segment elevation MI.

Conflict of interest statement

Disclosure: DB has received grants from the British Heart Foundation (PG 10/71/28462) and Wellcome (ISSF 204809/Z/16/Z) and honoraria from Astra Zeneca, Pfizer and Vifor Pharma. All other authors have no conflicts of interest to declare.

Copyright © 2019, Radcliffe Cardiology.

Figures

Figure 1:. Diagnostic Algorithm for Symptoms of…
Figure 1:. Diagnostic Algorithm for Symptoms of Acute Coronary Syndrome in Patients with an Abnormal Renal Profile

References

    1. Song D, de Zoysa JR, Ng A, Chiu W. Troponins in acute kidney injury. Ren Fail. 2012;34:35–9. doi: 10.3109/0886022X.2011.623440.
    1. Chung JZ, Dallas Jones GR. Effect of renal function on serum cardiac troponin T – population and individual effects. Clin Biochem. 2015;48:807–10. doi: 10.1016/j.clinbiochem.2015.05.004.
    1. Michos ED, Wilson LM, Yeh HC et al. Prognostic value of cardiac troponin in patients with chronic kidney disease without suspected acute coronary syndrome: a systematic review and meta-analysis. Ann Intern Med. 2014;161:491–501. doi: 10.7326/M14-0743.
    1. Susantitaphong P, Cruz DN, Cerda J et al. World incidence of AKI: a meta-analysis. Clin J Am Soc Nephrol. 2013;8:1482–93. doi: 10.2215/CJN.00710113.
    1. Hsu RK, McCulloch CE, Dudley RA, Lo LJ, Hsu CY. Temporal changes in incidence of dialysis-requiring AKI. J Am Soc Nephrol. 2013;24:37–42. doi: 10.1681/ASN.2012080800.
    1. Haraldsson B. Nyström J, Deen WM. Properties of the glomerular barrier and mechanisms of proteinuria. Physiol Rev. 2008;88:451–87. doi: 10.1152/physrev.00055.2006.
    1. Christensen EI, Birn H. Megalin and cubilin: synergistic endocytic receptors in renal proximal tubule. Am J Physiol Renal Physiol. 2001;280:F562–73. doi: 10.1152/ajprenal.2001.280.4.F562.
    1. Collinson PO, Garrison L, Christenson RH. Cardiac biomarkers - A short biography. Clin Biochem. 2015;48:197–200. doi: 10.1016/j.clinbiochem.2014.11.014.
    1. deFilippi C, Seliger S. The cardiac troponin renal disease diagnostic conundrum: past, present, and future. Circulation. 2018;137:452–454. doi: 10.1161/CIRCULATIONAHA.117.031717.
    1. Babuin L, Jaffe A. Troponin: the biomarker of choice for the detection of cardiac injury. CMAJ. 2005;173:1191–202. doi: 10.1503/cmaj/051291.
    1. McLaurin MD, Apple FS, Voss EM et al. Cardiac troponin I, cardiac troponin T, and creatine kinase MB in dialysis patients without ischemic heart disease: evidence of cardiac troponin T expression in skeletal muscle. Clin Chem. 1997;43:976–82.
    1. Apple FS, Ricchiuti C, Voss EM. Expression of cardiac troponin T isoforms in skeletal muscle of renal disease patients will not cause false-positive serum results by the second generation cardiac troponin T assay. Eur Heart J. 1998;19:N30–3. (Suppl N)
    1. Thygesen K, Alpert JS, Jaffe AS et al. Third universal definition of myocardial infarction. J Am Coll Cardiol. 2012;60:1581–98. doi: 10.1016/j.jacc.2012.08.001.
    1. Bjurman C, Petzold M, Venge P et al. High-sensitive cardiac troponin, NT-proBNP, hFABP and copeptin levels in relation to glomerular filtration rates and a medical record of cardiovascular disease. Clin Biochem. 2015;48:302–7. doi: 10.1016/j.clinbiochem.2015.01.008.
    1. Roberts MA, Hedley AJ, Ierino F. Understanding cardiac biomarkers in end-stage kidney disease: frequently asked questions and the promise of clinical application. Nephrology (Carlton) 2011;16:251–60. doi: 10.1111/j.1440-1797.2010.01413.x.
    1. Twerenbold R, Wildi K, Jaeger C et al. Optimal cutoff levels of more sensitive cardiac troponin assays for the early diagnosis of myocardial infarction in patients with renal dysfunction. Circulation. 2015;131:2041–50. doi: 10.1161/CIRCULATIONAHA.114.014245.
    1. Morrow DA, Bonaca MP. Real-world application of ‘delta’ troponin: diagnostic and prognostic implications. J Am Coll Cardiol. 2013;62:1239–41. doi: 10.1016/j.jacc.2013.06.049.
    1. Roffi M, Patrono C, Collet JP et al. 2015 ESC guidelines for the management of acute coronary syndromes in patients presenting without persistent ST-segment elevation. Eur Heart J. 2016;37:267–315. doi: 10.1093/eurheartj/ehv320.
    1. Miller-Hodges E, Anand A, Shah ASV et al. High-sensitivity cardiac troponin and the risk stratification of patients with renal impairment presenting with suspected acute coronary syndrome. Circulation. 2018;137:425–35. doi: 10.1161/CIRCULATIONAHA.117.030320.
    1. Twerenbold R, Badertscher P, Boeddinghaus J et al. 0/1-hour triage algorithm for myocardial infarction in patients with renal dysfunction. Circulation. 2018;137:436–51. doi: 10.1161/CIRCULATIONAHA.117.028901.
    1. Amin AP, Salisbury AC, McCullough PA et al. Trends in the incidence of acute kidney injury in patients hospitalized with acute myocardial infarction. Arch Intern Med. 2012;172:246–53. doi: 10.1001/archinternmed.2011.1202.
    1. Chapman AR, Adamson PD, Mills NL. Assessment and classification of patients with myocardial injury and infarction in clinical practice. Heart. 2017;103:10–8. doi: 10.1136/heartjnl-2016-309530.
    1. Collinson PO, Hadcocks L, Foo Y et al. Cardiac troponins in patients with renal dysfunction. Ann Clin Biochem. 1998;35:380–6. doi: 10.1177/000456329803500306.
    1. Thygesen K, Alpert JS, Jaffe AS et al. Fourth Universal Definition of Myocardial Infarction (2018) Circulation. 2018;138:e618–e651. doi: 10.1161/CIR.0000000000000617.

Source: PubMed

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