Persistent Severe Acute Kidney Injury Among Critically Ill Patients: Outcomes and Predictive Markers-A Single-Center...

Persistent severe acute kidney injury (PS-AKI)-recently standardized as Kidney Disease: Improving Global Outcomes (KDIGO) Stage 3 persisting ≥ 72 h, or renal replacement therapy/death after Stage 3 diagnosis-has emerged as a trajectory-based phenotype complementing conventional KDIGO staging. Evidence in contemporary intensive care unit (ICU) cohorts remains limited.

We retrospectively studied adults admitted to a tertiary ICU (January 2024-June 2025). Acute kidney injury (AKI) was staged per KDIGO 2012, with trajectories classified as Stage 1 AKI, transient AKI (Stage 2-3 resolving within 48 h), persistent mild-moderate AKI, or PS-AKI. The primary outcome was in-hospital mortality; secondary outcomes included renal recovery. Predictors of PS-AKI were explored using logistic regression and gradient boosting with SHAP attribution.

Among 139 ICU patients with AKI screened, 106 met criteria. Most AKI was community-acquired (97/106, 91.5%). PS-AKI accounted for 23% (24/106) and carried the worst outcomes, with in-hospital mortality 54% and renal recovery 17%. Within Stage 2-3, PS-AKI was associated with substantially worse outcomes than non-PS trajectories (mortality 54% vs 10.8%; adjusted HR for death 2.23, 95% CI 0.69-7.21; adjusted OR for renal recovery 0.07, 95% CI 0.01-0.24). A 72-h landmark analysis showed similar but nonsignificant trends. Inflammatory profiles distinguished PS-AKI, with higher neutrophil-to-lymphocyte ratio (NLR), C-reactive protein (CRP), and lower platelets. The composite NLR-to-platelet ratio (NLR/PLT) was independently associated with PS-AKI (adjusted OR 2.51 per doubling, 95% CI 1.52-4.12; AUC 0.86), while the systemic immune-inflammation index (SII) showed no significant association.

In this predominant community-acquired ICU cohort, PS-AKI was common and strongly associated with poor in-hospital outcomes. The co-occurrence of inflammation and thrombocytopenia, summarized by NLR/PLT, may represent a simple exploratory signal for early-risk appraisal. These findings support further research into trajectory-based AKI phenotypes and the potential utility of inflammation-hematologic markers in predicting persistence.