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Renal Replacement Therapy / Acute Kidney Injury / Sodium-glucose Transporter 2 Inhibitors · Journal article
Journal of Critical Care · July 31, 2026
Encouraging direction, but not yet definitive.
This post-hoc analysis of 212 critically ill patients with AKI found no safety signal or clinical benefit for dapagliflozin initiation compared to control over 28 days, with overlapping confidence intervals and physiological stability in both arms. Likelihood ratios at a 5% absolute effect threshold do not exclude moderate harm or benefit, indicating the sample is too small to draw definitive conclusions and supporting feasibility of dedicated prospective trials.
Post-hoc subgroup analysis of a randomized controlled trial. Critically ill patients with acute kidney injury enrolled in the DEFENDER trial; 100 allocated to dapagliflozin and 112 to control.. Intervention: Dapagliflozin initiation (dose not specified in abstract).. Compared with: Standard care (control).. n = 212. Not stated in source text..
28-day mortality: 38% (dapagliflozin) vs 40% (control), adjusted risk difference −1.9% (95% CI −14.5 to 10.7) Kidney replacement therapy: 12% vs 18%, adjusted risk difference −7.4% (95% CI −16.2 to 1.5) Composite death/KRT: 41% vs 42%, adjusted risk difference −0.9% (95% CI −13.6 to 11.8)
Likelihood ratios at 5% threshold provide limited separation, meaning moderate harm or benefit cannot be ruled out. Duration of follow-up (28 days) and physiological assessment window (days 1–5) may not detect delayed or longer-term harms.
Clinicians should view this as reassuring evidence that dapagliflozin initiation does not appear to cause acute hemodynamic or metabolic harm in critically ill AKI patients, but should not interpret near-neutral results as proof of efficacy. The wide confidence intervals and weak likelihood ratios indicate a dedicated prospective trial is needed before recommending routine use in this population.
A post-hoc analysis from a controlled trial showing no safety signal for dapagliflozin in critically ill AKI patients, with near-neutral effects and physiological stability, but underpowered to detect clinically meaningful benefit or harm.
As stated by the source record.
Quoted from the source exactly as published.
Clinicians should view this as reassuring evidence that dapagliflozin initiation does not appear to cause acute hemodynamic or metabolic harm in critically ill AKI patients, but should not interpret near-neutral results as proof of efficacy. The wide confidence intervals and weak likelihood ratios indicate a dedicated prospective trial is needed before recommending routine use in this population.
Graded across the dimensions that decide whether you should act, each from what the source actually supports. There is no single score, and where a dimension was not assessed it says so.
Background. SGLT2 inhibitor use in acute kidney injury (AKI) is controversial due to concerns about hemodynamic instability. We evaluated dapagliflozin initiation in critically ill patients with AKI enrolled in the DEFENDER trial.Methods. Among 212 patients with AKI at enrollment (100 dapagliflozin, 112 control), we compared 28-day mortality, kidney replacement therapy (KRT), and composite death/KRT. Adjusted risk differences were estimated controlling for age, sepsis, baseline vasopressor use, and creatinine. Physiological trajectories (creatinine, urine output, fluid balance, acid-base parameters) over days 1-5 were analyzed using mixed models. Likelihood ratios quantified compatibility with clinically meaningful harm or benefit.Results. Event rates were similar: 28-day mortality 38% vs 40%, KRT 12% vs 18%, composite 41% vs 42% (dapagliflozin vs control). Adjusted risk differences were - 1.9% (95% CI -14.5 to 10.7) for death, -7.4% (-16.2 to 1.5) for KRT, and - 0.9% (-13.6 to 11.8) for the composite. Physiological trajectories showed no divergence suggestive of hemodynamic or metabolic instability. Likelihood ratios provided limited separation: at 5% absolute effect threshold, LR against harm was 1.47 and against benefit 1.19.Conclusions. Dapagliflozin initiation in critically ill patients with AKI was not associated with excess mortality, KRT, or physiological derangement. The near-neutral evidential profile indicates neither moderate harm nor benefit can be excluded, supporting feasibility of dedicated trials of SGLT2 inhibitors in AKI.
Taken from the source record, never inferred. Follow any of these and new work involving them reaches your briefing.