The utility of conventional upper reference limits (URL) for N-terminal pro brain natriuretic peptide (NT-proBNP) and high-sensitivity cardiac troponin T (hsTnT) in chronic kidney disease (CKD) remains debated. We analyzed the distribution of hsTnT and NT-proBNP in people with CKD in ambulatory settings to examine the diagnostic value of conventional URL in this population.
Observational study.
We studied participants of the Chronic Renal Insufficiency Cohort with CKD and no self-reported history of cardiovascular disease (CVD).
Estimated glomerular filtration rate (eGFR).
NT-proBNP and hsTnT at baseline.
We described the proportion of participants above the conventional URL for NT-proBNP (125 pg/ml) and hsTnT (14 ng/L) overall, and by eGFR. We then estimated 99 percentile URL for NT-proBNP and hsTnT. Using quantile regression of the 99 percentile, we modeled the association of eGFR with NT-proBNP and hsTnT.
Among 2,312 CKD participants, 40% and 43% had levels of NT-proBNP and hsTnT above conventional URL, respectively. In those with eGFR<30 ml/min/1.73 m, 71% and 68% of participants had concentrations of NT-proBNP and hsTnT above conventional URL, respectively. Amongst all CKD participants, the 99 percentile for NT-proBNP was 3,592(95% CI: 2,470, 4,849) pg/mL and for hsTnT was 126(95% CI: 100, 144) ng/L. Each 15 ml/min/1.73 m decrement in eGFR was associated with a ∼40% higher threshold for the 99 percentile of NT-proBNP [1.43 (1.21, 1.69)] and hsTnT [1.45 (1.31, 1.60)].
Study included ambulatory patients; we could not test the accuracy of upper reference limits of NT-proBNP and hsTnT in the acute care setting.
In this ambulatory CKD population with no self-reported history of CVD, a range of 40-88% of participants had concentrations of NT-proBNP and hsTnT above conventional URL, depending on eGFR strata. Developing eGFR-specific thresholds for these commonly-used cardiac biomarkers in the setting of CKD may improve their utility for evaluation of suspected heart failure and myocardial infarction.

Copyright © 2021. Published by Elsevier Inc.

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