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PurposeThe Acute Disease Quality Initiative (ADQI) Workgroup recently released a consensus definition of sepsis-associated acute kidney injury (SA-AKI), combining Sepsis-3 and Kidney Disease Improving Global Outcomes (KDIGO) AKI criteria. This study aims to describe the epidemiology of SA-AKI.MethodsThis is a retrospective cohort study carried out in 12 intensive care units (ICUs) from 2015 to 2021. We studied the incidence, patient characteristics, timing, trajectory, treatment, and associated outcomes of SA-AKI based on the ADQI definition.ResultsOut of 84,528 admissions, 13,451 met the SA-AKI criteria with its incidence peaking at 18% in 2021. SA-AKI patients were typically admitted from home via the emergency department (ED) with a median time to SA-AKI diagnosis of 1 day (interquartile range (IQR) 1–1) from ICU admission. At diagnosis, most SA-AKI patients (54%) had a stage 1 AKI, mostly due to the low urinary output (UO) criterion only (65%). Compared to diagnosis by creatinine alone, or by both UO and creatinine criteria, patients diagnosed by UO alone had lower renal replacement therapy (RRT) requirements (2.8% vs 18% vs 50%; p < 0.001), which was consistent across all stages of AKI. SA-AKI hospital mortality was 18% and SA-AKI was independently associated with increased mortality. In SA-AKI, diagnosis by low UO only, compared to creatinine alone or to both UO and creatinine criteria, carried an odds ratio of 0.34 (95% confidence interval (CI) 0.32–0.36) for mortality.ConclusionSA-AKI occurs in 1 in 6 ICU patients, is diagnosed on day 1 and carries significant morbidity and mortality risk with patients mostly admitted from home via the ED. However, most SA-AKI is stage 1 and mostly due to low UO, which carries much lower risk than diagnosis by other criteria.

Background In septic shock, the optimal timing of adjunctive vasopressin initiation shock is unknown. We aimed to assess the effect of its early initiation for patients with septic shock. Methods We conducted a multicenter target trial emulation to estimate the intensive care unit (ICU) mortality effect of early (≤ 6 h) adjunctive vasopressin compared with usual care. Eligible patients had septic shock diagnosed within 6 h of ICU admission. The primary outcome of this study was 30-day ICU mortality. Subgroup analyses were conducted to test the interaction of early vasopressin start with peak norepinephrine-equivalent dose (NED) at 6 h, APACHE score, peak lactate at 6 h and invasive mechanical ventilation. Secondary outcomes were the impact of delayed vasopressin introduction on 30-day ICU mortality and effect of NED at vasopressin start on 30-day ICU mortality. We used the parametric g-formula to emulate a target trial. Results Overall, 3,105 patients fulfilled the inclusion criteria. Mean age was 62 years and mean APACHE III score was 83. In the first six hours of vasopressor therapy, 1,864 (60%) patients were invasively ventilated. Estimated 30-day ICU mortality was 19.34% (95%CI, 17.0 to 21.68) in the no vasopressin group and 18.45% (95%CI, 16.26 to 20.63) in the early vasopressin group; relative risk 0.95 (95%CI, 0.93 to 0.98). The estimated 30-day ICU mortality effect of starting vasopressin was particularly strong at lower norepinephrine doses (< 0.25 µg.kg −1 .min −1 ) and significant at lower norepinephrine doses than recommended by the Surviving Sepsis Campaign Guidelines. Vasopressin administration progressively increased over the study period, from 35.2% (95%CI, 30.0 to 40.5) in 2015 to 45.1% (95%CI, 40.7 to 49.6) in 2021 (ß =  + 1.3% per year; 95%CI, + 0.46 to + 2.16, p  = 0.011). Patients had progressively lower norepinephrine equivalent dose (ß = − 0.05 µg.kg −1 .min −1 per year; 95%CI, − 0.09 to − 0.002, p  = 0.038) and lower total SOFA score (ß = − 0.1 point per year; 95%CI, − 0.18 to − 0.07, p  < 0.001) at vasopressin start. Conclusions In this emulation of a hypothetical target trial, patients with septic shock benefited from early vasopressin administration. These findings can help design prospective randomised-control trials of early adjunctive vasopressin use in septic shock.

In critically ill patients with acute kidney injury (AKI), a fluid balance (FB) > 2 L at 72 h after AKI diagnosis is associated with adverse outcomes. Identification of patients at high-risk for such fluid accumulation may help prevent it. We used Australian electronic medical record (EMR)-based clinical data to develop the “AKI-FB risk score”, validated it in a British cohort and used it to predict a positive FB >2 L at 72 h after AKI diagnosis. We developed the AKI-FB score in 32,030 patients with a median age of 63 years and a median APACHE 2 score of 16. We validated it in 4465 patients, with significant differences in admission diagnoses and interventions. The key score variables were admission after trauma, sepsis or septic shock, and, on the day of AKI diagnosis, highest creatinine, daily cumulative FB, mechanical ventilation, noradrenaline use, noradrenaline equivalent dose >0.07 μg/kg/min, lactate ≥2 mmol/L, transfusion, and nutritional support. A score threshold of 32 had a sensitivity of 75 % and a specificity of 72 % for predicting a > 2 L positive FB with an AUC-ROC of 0.805; 95 % CI 0.799 to 0.810. External validation demonstrated an AUC of 0.761 (95 % CI 0.746 to 0.775). We developed and validated the “AKI-FB risk score” to predict patients who developed a positive FB >2 L within 72 h of AKI diagnosis. This prediction score was robust and facilitated the identification of high-risk AKI patients who could be the tarted for preventive measures and be included in future clinical trials of FB management. •Developed AKI-FB risk score for the prediction of a strongly positive fluid balance 72 hours after diagnosis of AKI.•The AKI-FB risk score had excellent predictive ability and was validated in a large cohort from another country.•A score of 32 or higher had high sensitivity and specificity for a positive fluid balance greater than 2L at 72 hours.