Timing of acute kidney injury in infarction-related cardiogenic shock : early onset signals a high-risk phenotype : a retrospective observational study

Abstract

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. Keywords: Acute kidney injury; cardiogenic shock; myocardial infarction; AKI timing; early-onset AKI; hemodynamic instability; lactate; renal dysfunction; in-hospital mortality