TOPLINE:

In infarct-related cardiogenic shock, acute kidney injury (AKI) occurring within 48 hours was identified as a high-risk haemodynamic phenotype — marked by severe haemodynamic instability, metabolic stress, and substantially increased in-hospital mortality.

METHODOLOGY:

• Researchers conducted a retrospective study of 369 patients (mean age, 69.2 years; 33.1% women) with infarct-related cardiogenic shock to investigate the association between the timing of AKI onset and patient characteristics, treatment intensity, and clinical outcomes.
• A total of 143 (38.8%) patients developed AKI within 96 hours, of whom 81 (56.6%) had early-onset AKI (≤ 48 hours) and 62 (43.4%) had late-onset AKI (> 48-96 hours).
• Infarct-related cardiogenic shock was defined by systolic blood pressure below 90 mm Hg for at least 30 minutes or the need for vasopressor support, signs of end-organ hypoperfusion, and a diagnosis of acute myocardial infarction.
• Serum creatinine measurements were required to be available during the first 96 hours of ICU admission to enable the accurate classification of AKI onset.
• The primary outcome was in-hospital mortality, and secondary outcomes included the severity of AKI (stages 1-3), need for renal replacement therapy, duration of mechanical ventilation, and norepinephrine dosage over time.

TAKEAWAY:

• Early-onset vs late-onset AKI was associated with increased serum creatinine concentrations at baseline (P = .048) and lactate concentrations at admission and 24 hours (P = .032 for both), greater norepinephrine requirements at 24 hours (P = .044), and more frequent mechanical ventilation (P = .011).
• In-hospital mortality was significantly higher in patients with early-onset AKI than in those with late-onset AKI (71.6% vs 54.8%; P = .018).
• Patients with early-onset AKI required renal replacement therapy more often (29.6% vs 16.1%; P = .037) and had a longer duration of ventilatory support (median, 194 vs 128 hours; P = .02) than those with late-onset AKI.
• Increased serum creatinine concentrations at baseline (adjusted odds ratio [aOR], 5.68 per mg/dL; P = .008) and elevated serum lactate concentrations at 24 hours (aOR, 2.67 per mmol/L; P < .001) were identified as independent predictors of early-onset AKI; early-onset AKI was independently associated with increased odds of in-hospital mortality (aOR, 2.12; P = .015).

IN PRACTICE:

"Early-onset AKI — particularly within 48 h — defines a high-risk phenotype marked by severe hemodynamic instability, metabolic stress, and substantially increased in-hospital mortality," the authors wrote.

"These findings support incorporating AKI timing into clinical risk models and underscore the need for early recognition and tailored renoprotective strategies to improve outcomes in this vulnerable population," they added.

SOURCE:

This study was led by Priyanka Boettger, Critical Care Medicine, Justus-Liebig University, Giessen, Germany. It was published online on January 06, 2026, in BMC Nephrology.

LIMITATIONS:

The single-centre design of this study may have limited generalisability. The retrospective design prevented causal inference. Daily rather than continuous serum creatinine measurements may have affected the precise timing classification of AKI onset.

DISCLOSURES:

This study did not receive any external funding. The authors declared having no competing interests.

This article was created using several editorial tools, including AI, as part of the process. Human editors reviewed this content before publication.