TY - JOUR
T1 - The influence of kidney function on the prognostic value of cardiac troponin
AU - Hasselbalch, Rasmus Bo
AU - Schultz, Martin
AU - Carlson, Nicholas
AU - Strandkjær, Nina
AU - Knudsen, Sophie Sander
AU - Kronborg, Alexander Holst
AU - Kragholm, Kristian H
AU - Andersen, Mikkel Porsborg
AU - Bundgaard, Henning
AU - Torp-Pedersen, Christian
AU - Aakre, Kristin M
AU - Iversen, Kasper Karmark
N1 - Copyright © 2025. Published by Elsevier Inc.
PY - 2026/1
Y1 - 2026/1
N2 - BACKGROUND: Kidney function influences the concentration of cardiac troponin T (cTnT) and I (cTnI). We investigate how this impacts their prognostic ability.METHODS: This Danish nationwide study included patients from 2013 to 2023 with at least two measurements of Roche hs-cTnT, Abbott hs-cTnI, or Siemens hs-cTnI Vista or Atellica during the index admission. Patients were stratified by estimated glomerular filtration rate (eGFR). We assessed prognostic ability by Cox models and area under the receiver operating characteristics curve (AUC). The primary endpoint was 30-day all-cause mortality.RESULTS: We included 277,723 patients (median age 69 years, 38.4 % female) of whom 19,565 (7.0 %) died within 30 days. Almost all patients with eGFR <30 ml/min/1.73 m2 had myocardial injury using hs-cTnT (99.4 %) compared to hs-cTnI (85.4 %). Hazard ratios (HRs) for overall myocardial injury were higher than for acute myocardial injury and declined with worsening eGFR, particularly for hs-cTnT: HR 15.58 (95 % CI 12.77-19.00) for eGFR ≥90 ml/min/1.73 m2, while estimation was impossible at eGFR 15-30 ml/min/1.73 m2 due to few normal values. The highest HR for acute myocardial injury at eGFR ≥90 ml/min/1.73 m2 was for hs-cTnI Abbott, HR 3.50 (95 % CI 2.79-4.38). AUC decreased with worsening eGFR across assays, 0.68-0.76 for eGFR ≥90 ml/min/1.73 m2 to 0.59-0.63 for eGFR <15 ml/min/1.73 m2. At eGFR ≥90 ml/min/1.73 m2 the optimal cutoff was 16.5 ng/l for hs-cTnT and below the sex-specific 99th percentile for all hs-cTnI assays, increasing 5-20-fold with lower eGFR for all assays.CONCLUSION: Kidney function affects cTn prognostic performance, with reduced predictive ability and higher optimal cutoff concentrations for lower eGFR.
AB - BACKGROUND: Kidney function influences the concentration of cardiac troponin T (cTnT) and I (cTnI). We investigate how this impacts their prognostic ability.METHODS: This Danish nationwide study included patients from 2013 to 2023 with at least two measurements of Roche hs-cTnT, Abbott hs-cTnI, or Siemens hs-cTnI Vista or Atellica during the index admission. Patients were stratified by estimated glomerular filtration rate (eGFR). We assessed prognostic ability by Cox models and area under the receiver operating characteristics curve (AUC). The primary endpoint was 30-day all-cause mortality.RESULTS: We included 277,723 patients (median age 69 years, 38.4 % female) of whom 19,565 (7.0 %) died within 30 days. Almost all patients with eGFR <30 ml/min/1.73 m2 had myocardial injury using hs-cTnT (99.4 %) compared to hs-cTnI (85.4 %). Hazard ratios (HRs) for overall myocardial injury were higher than for acute myocardial injury and declined with worsening eGFR, particularly for hs-cTnT: HR 15.58 (95 % CI 12.77-19.00) for eGFR ≥90 ml/min/1.73 m2, while estimation was impossible at eGFR 15-30 ml/min/1.73 m2 due to few normal values. The highest HR for acute myocardial injury at eGFR ≥90 ml/min/1.73 m2 was for hs-cTnI Abbott, HR 3.50 (95 % CI 2.79-4.38). AUC decreased with worsening eGFR across assays, 0.68-0.76 for eGFR ≥90 ml/min/1.73 m2 to 0.59-0.63 for eGFR <15 ml/min/1.73 m2. At eGFR ≥90 ml/min/1.73 m2 the optimal cutoff was 16.5 ng/l for hs-cTnT and below the sex-specific 99th percentile for all hs-cTnI assays, increasing 5-20-fold with lower eGFR for all assays.CONCLUSION: Kidney function affects cTn prognostic performance, with reduced predictive ability and higher optimal cutoff concentrations for lower eGFR.
KW - Cardiac troponin
KW - Coronary artery disease
KW - Kidney function
KW - Risk prediction
UR - https://www.scopus.com/pages/publications/105025029680
U2 - 10.1016/j.clinbiochem.2025.111068
DO - 10.1016/j.clinbiochem.2025.111068
M3 - Journal article
C2 - 41412456
SN - 0009-9120
VL - 141
JO - Clinical Biochemistry
JF - Clinical Biochemistry
M1 - 111068
ER -