Understanding cardiac biomarkers in end‐stage kidney disease: Frequently asked questions and the promise of clinical application

Roberts, Matthew A; Hedley, Adam J; Ierino, Francesco L.

doi:10.1111/j.1440-1797.2010.01413.x

Cited by 14 publications

(10 citation statements)

References 117 publications

(186 reference statements)

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“…All samples in this study were collected just before the hemodialysis procedure to eliminate effects of this procedure (19,20). Studies of the effect of vascular access creation on BNP concentrations are inconclusive (21,22), and studies of BNP as a biomarker of volume overload in patients receiving dialysis also vary in their conclusions (15,16,18).…”

Section: Discussionmentioning

confidence: 99%

Temporal Trajectory of B-Type Natriuretic Peptide in Patients with CKD Stages 3 and 4, Dialysis, and Kidney Transplant

Roberts

Hare

Sikaris³

et al. 2014

Clinical Journal of the American Society of Nephrology

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Background and objectives B-type natriuretic peptide (BNP) concentration predicts outcome in patients undergoing dialysis. Because survival and cardiovascular risk change across the CKD continuum, serial changes in BNP were compared in patients at different CKD stages and after kidney transplantation.Design, setting, participants, & measurements Patients with CKD stages 3 and 4 (CKD 3-4), dialysis patients, and kidney transplant recipients (KTRs) from one center had two measurements of BNP taken a median of 161 days apart in 2003-2004 and were followed until July 2012. Both BNP-32 (Triage BNP; Biosite Diagnostics) and NT-BNP-76 (proBNP; Roche Diagnostics) were assayed. The interaction between change in log-transformed BNP concentration over time and patient group was tested by fitting regression models on panel data with random effects. Survival after the second measurement was compared by tertile of change in BNP.Results Patients with CKD 3-4 (n=48), dialysis patients (n=102), and KTRs (n=73) were followed for a median of 5.7, 4.8, and 5.9 years, respectively. The interaction between patient group and BNP measurements over time was significant for NT-BNP-76 (P,0.001) and BNP-32 (P,0.01). Median NT-BNP-76 increased in dialysis patients and those with CKD 3-4 from 3850 pg/ml (interquartile range [IQR], 1776-12,323 pg/ml) to 18,830 pg/ml (IQR, 6114-61,009 pg/ml; P,0.001) and from 698 pg/ml (IQR, 283-2922 pg/ml) to 2529 pg/ml (IQR, 347-9277 pg/ml; P=0.002), respectively. Change was not significant for KTRs or comparisons made with BNP-32. Survival rate was significantly lower for patients with the highest tertile of change in NT-BNP-76 among patients with CKD 3-4 (P=0.02), but not in the dialysis or KTR groups. In 11 patients who received a kidney transplant during the study, median NT-BNP-76 decreased from 9607 pg/ml (IQR, 2292-31,282 pg/ml) to 457 pg/ml (IQR, 203-863 pg/ml) after transplant (P,0.01).Conclusions The temporal trajectory of BNP differs between dialysis patients and those with CKD 3-4 and KTRs. This has important implications for the development of BNP-guided management strategies in CKD.

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Section: Discussionmentioning

confidence: 99%

Temporal Trajectory of B-Type Natriuretic Peptide in Patients with CKD Stages 3 and 4, Dialysis, and Kidney Transplant

Roberts

Hare

Sikaris³

et al. 2014

Clinical Journal of the American Society of Nephrology

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“…22 In general, lowering of cardiac biomarkers such as BNP and the troponins appears more likely if high-flux membranes are used, 23 but highsensitivity troponin assays have only recently been studied. 24 Galectin-3, at 32-35 kDa 25 is similar in size to the troponins and larger than BNP, 23 suggesting that it should be more difficult to remove with dialysis. Despite this, levels of galectin-3, but not the other markers, are about 50% lower after dialysis compared to before; this should be considered in interpreting levels or comparing values between studies.…”

Section: Discussionmentioning

confidence: 99%

“…and median (interquartile range) dialysis duration 13.6 (9.8-19.1) months participated. Galectin-3 was substantially lower following haemodialysis: 55 ng/mL (47-70) versus 23 ng/mL (19)(20)(21)(22)(23)(24)(25)(26)(27), P < 0.001), but other biomarkers changed little. By increasing RRF tertile, post-dialysis galectin-3 was 32.6 ng/mL (23.7-36.6), 21.9 ng/mL (19.0-23.2) and 19.0 ng/mL (16.9-21.0, P = 0.001);…”

mentioning

confidence: 91%

Effect of haemodialysis and residual renal function on serum levels of galectin‐3, B‐type natriuretic peptides and cardiac troponin T

et al. 2018

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“…13 However, chronic, stable, elevated troponin concentrations have been demonstrated in the CKD population in the absence of any clinical evidence of a myocardial ischaemic event. 16 Perhaps the most commonly adopted approach to this problem is to look for a change of more than 20% between two values taken several hours apart, although there is no real evidence to support this strategy and there is a potential to underestimate myocardial events. 17 The European Society of Cardiology (ESC) recommends an algorithm to rapidly rule in or rule out NSTEMI using high-sensitivity cardiac troponin concentrations, regardless of renal function.…”

Section: Cardiac Troponins In Chronic Kidney Disease and End-stage Kimentioning

confidence: 99%

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

2019

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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.

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Understanding cardiac biomarkers in end‐stage kidney disease: Frequently asked questions and the promise of clinical application

Cited by 14 publications

References 117 publications

Temporal Trajectory of B-Type Natriuretic Peptide in Patients with CKD Stages 3 and 4, Dialysis, and Kidney Transplant

Temporal Trajectory of B-Type Natriuretic Peptide in Patients with CKD Stages 3 and 4, Dialysis, and Kidney Transplant

Effect of haemodialysis and residual renal function on serum levels of galectin‐3, B‐type natriuretic peptides and cardiac troponin T

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

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