BMC nephrology · 2026
Timing of acute kidney injury in infarction-related cardiogenic shock: early onset signals a high-risk phenotype - a retrospective observational study.
СтатьяНаблюдательное исследованиеНазвание и аннотация: Перевод в очереди
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Boettger Priyanka, Preusse-Sondermann Henriette, Sedighi Jamschid, Jobst Jannik, Hassan Hassan, Bayram Utku, Piayda Kerstin, Janusch Matthias, Assmus Birgit, Unsoeld Bernhard, Lemm Henning, Sossalla Samuel, Buerke Michael
Аннотация
BACKGROUND: Acute kidney injury (AKI) is common in cardiogenic shock (CS) and increases mortality, but the prognostic impact of onset timing in infarct-related CS is unclear. We examined whether early versus late AKI onset is associated with differences in patient characteristics and outcomes.
METHODS: In this retrospective observational study, 369 patients with infarct-related CS were classified by AKI timing within the first 96 h of admission: early (≤ 48 h) or late (> 48 h), according to KDIGO criteria. Clinical, hemodynamic, and inflammatory parameters and outcomes were compared. Multivariable logistic regression identified independent predictors of early AKI and in-hospital mortality.
RESULTS: AKI occurred in 143 patients (38.8%), with 56.6% early-onset. In-hospital mortality was higher with early AKI than late AKI (71.6% vs. 54.8%; absolute difference 16.8%, 95% CI 3.1-30.5; p = 0.018). Early AKI patients had higher lactate at admission (median 4.3 vs. 3.1 mmol/L; p = 0.028), greater norepinephrine requirements (0.34 vs. 0.21 µg/kg/min; p = 0.044), and more frequent mechanical ventilation (81.5% vs. 61.3%; p = 0.011). In multivariable analysis, early AKI independently predicted in-hospital mortality (adjusted OR 2.12, 95% CI 1.16-3.87; p = 0.015), and was associated with baseline creatinine (OR 5.68 per 1 mg/dL, p = 0.008) and 24-h lactate (OR 2.67 per mmol/L, p < 0.001).
CONCLUSIONS: In infarct-related CS, AKI within 48 h marks a high-risk hemodynamic phenotype with markedly increased mortality, driven by renal vulnerability and early hypoperfusion. Incorporating AKI timing into risk stratification may help target early renoprotective interventions.
METHODS: In this retrospective observational study, 369 patients with infarct-related CS were classified by AKI timing within the first 96 h of admission: early (≤ 48 h) or late (> 48 h), according to KDIGO criteria. Clinical, hemodynamic, and inflammatory parameters and outcomes were compared. Multivariable logistic regression identified independent predictors of early AKI and in-hospital mortality.
RESULTS: AKI occurred in 143 patients (38.8%), with 56.6% early-onset. In-hospital mortality was higher with early AKI than late AKI (71.6% vs. 54.8%; absolute difference 16.8%, 95% CI 3.1-30.5; p = 0.018). Early AKI patients had higher lactate at admission (median 4.3 vs. 3.1 mmol/L; p = 0.028), greater norepinephrine requirements (0.34 vs. 0.21 µg/kg/min; p = 0.044), and more frequent mechanical ventilation (81.5% vs. 61.3%; p = 0.011). In multivariable analysis, early AKI independently predicted in-hospital mortality (adjusted OR 2.12, 95% CI 1.16-3.87; p = 0.015), and was associated with baseline creatinine (OR 5.68 per 1 mg/dL, p = 0.008) and 24-h lactate (OR 2.67 per mmol/L, p < 0.001).
CONCLUSIONS: In infarct-related CS, AKI within 48 h marks a high-risk hemodynamic phenotype with markedly increased mortality, driven by renal vulnerability and early hypoperfusion. Incorporating AKI timing into risk stratification may help target early renoprotective interventions.