Summary of a lecture presented by Dr. Ravindra Mehta during ICU Essentials 2025 Webinar Summary: Sepsis, AKI, and Smart Fluid Management
Sepsis accounts for up to 41% of all AKI cases, and approximately 57% of ICU patients with AKI present with a sepsis-related component. These complications are particularly common in elderly, female, or comorbid patients.
Diagnostic criteria based on KDIGO standards emphasize serum creatinine (SCr) and urine output (UO). AKI phenotypes differ by timing and duration: early AKI occurs within 48 hours of sepsis onset, while late AKI appears afterward.
Transient AKI resolves quickly, often within days; persistent AKI lasts beyond 48–72 hours and is linked to longer ICU stays and higher mortality. These distinctions guide both monitoring intensity and intervention strategies.
A Chinese ICU study visualized AKI progression using Sankey plots, showing that patients with early-persistent AKI had the poorest outcomes – underscoring the clinical impact of early detection and recovery trajectory.
The PICARD Study found similar mortality outcomes regardless of whether sepsis occurred before or after AKI onset. Meanwhile, data from Australia and New Zealand showed that AKI identified by urine output alone resulted in better recovery and fewer dialysis requirements (3.5%) compared to diagnoses based on SCr or combined criteria.
SA-AKI pathophysiology includes disrupted renal hemodynamics, immune activation, and mitochondrial injury. In experimental sheep models, angiotensin reversed efferent arteriole vasodilation and restored UO despite reduced total renal blood flow – highlighting that glomerular filtration depends not just on flow, but on arteriole tone balance.
Urine output was presented as a highly sensitive indicator of AKI. Both duration and frequency of oliguria correlate strongly with progression and mortality. A combined approach using functional markers (UO, SCr) and structural biomarkers (e.g., NGAL, TIMP2–IGFBP7) supports earlier and more targeted intervention.
