ArticleFrontiers in nephrology2026
Acute kidney injury, baseline renal function, troponin, and survival after myocardial infarction.
Article in Frontiers in nephrology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
Background: The roles of chronic kidney disease and acute kidney injury (AKI) as determinants of short- and long-term survival following myocardial infarction (MI) have not been well investigated. Methods: A retrospective analysis of electronic health record data was conducted for U.S. veterans between 2002 and 2015, with up to 15 years of follow-up after MI. Eligible participants included 49,150 veterans with a serum creatinine measurement prior to MI hospitalization. AKI stage was determined by the change between the pre-hospitalization creatinine level and the peak in-hospital measurement. The associations of AKI, estimated glomerular filtration rate (eGFR), and troponin I ratios with survival were evaluated using Cox proportional hazards models. Results: Compared to the no-AKI group, the hazard ratios (HRs) and 95% confidence intervals (CIs) for 30-day mortality were 3.12 (2.87-3.39), 5.12 (4.65-5.65), and 7.81 (6.93-8.81) across worsening stages of AKI. For 15-year mortality, the HRs were 1.76 (1.68-1.85), 2.33 (2.17-2.50), and 2.66 (2.37-2.99). Compared to those with eGFR >60 mL/min/1.73 m², HRs (95% CI) for 30-day mortality were 1.23 (1.13-1.33), 1.46 (1.33-1.59), and 1.92 (1.72-2.13) across decreasing eGFR levels. For 15-year mortality, HRs were 1.21 (1.17-1.25), 1.55 (1.49-1.61), and 2.13 (2.03-2.24). Mortality rates increased with rising troponin I (cTnI) ratios, particularly for 30-day mortality. Conclusions: AKI, baseline eGFR, and troponin levels were associated with both short- and long-term survival following MI. AKI during MI hospitalization was a particularly strong determinant of short-term mortality.
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