Key result
Top hs-cTnT quintile in AKI without MI is linked to ~9-fold higher in-hospital mortality and MACE.
Why the study?
Elevated and dynamic hs-cTnT concentrations are often observed in patients with AKI without MI, but their prognostic implications were unknown.
Does elevated high-sensitivity cardiac troponin T (hs-cTnT) predict mortality and MACE in patients with acute kidney injury without myocardial infarction?
Cohort (n=12,136)
Yes
Does elevated high-sensitivity cardiac troponin T (hs-cTnT) predict mortality and MACE in patients with acute kidney injury without myocardial infarction?
Effect estimate: aOR 8.68 (95% CI 6.85 to 11.0)
In patients with AKI but without acute MI, elevated peak hs-cTnT is strongly associated with increased short- and long-term mortality and MACE.
No takes yet. Share an insight, caveat, or question.
Elevated hs-cTnT in AKI without MI flags high-risk patients; extends prior associations but leaves open whether targeted interventions improve outcomes.
Cyon et al. (2025) conducted a cohort in Acute kidney injury without myocardial infarction (n=12,136). Peak high-sensitivity cardiac troponin T (hs-cTnT) vs. Lower hs-cTnT levels was evaluated on In-hospital mortality (aOR 8.68, 95% CI 6.85 to 11.0). In patients with AKI without MI, the highest quintile of peak hs-cTnT was associated with increased in-hospital mortality (aOR 8.68; 95% CI 6.85-11.0) and long-term MACE (HR 2.12; 95% CI 2.00-2.24).
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