#3372 HOST RESPONSE CHANGES ASSOCIATED WITH PERSISTENT ACUTE KIDNEY INJURY IN CRITICALLY ILL PATIENTS WITH COVID-19

Abstract Background and Aims In sepsis, the dysregulated host response has been, at least in part, linked to development of acute kidney injury (AKI) its duration. Data on COVID-19 persistent-AKI (duration > 48 h) critically ill patients are scarce. We hypothesized that infected who develop have different aberrations. To address this hypothesis, we sequentially measured immune biomarkers admitted intensive care unit (ICU). Method included ICU from two tertiary hospitals one primary hospital between March July 2020 (first wave). All had PCR-confirmed COVID-19. Excluded were readmitted patients, transfers another ICU, with chronic disease (CKD stage 3 or higher). The presence AKI was assessed by using hourly urine output daily serum creatinine levels, classified into stages according Kidney Disease: Improving Global Outcomes (KDIGO) criteria. a subset (n=113), 41 plasma protein Luminex platform ELISA, categorized five pathophysiological domains: systemic inflammation, endothelial cell activation dysfunction, coagulation activation, lung dysfunction. Mixed effects models used analyse longitudinal data. Results Of 185 admissions enrolled, 8 excluded because existing CKD. remaining 177 106 (59.9%) within first h admission; these, 76 (71.7%) persistent 30 (28.3%) transient AKI. Patients more often obese history hypertension. A higher severity – as determined sequential organ failure assessment (SOFA) score - observed group, which driven renal component non-renal SOFA similar no-AKI, transient-, Sequential biomarker analyses revealed significantly elevated compared transient-AKI four days, mainly related inflammation (triggering receptor expressed myeloid cells-1 [TREM-1], p=.003; tumour necrosis factor 1 [TNF-RI], p < 0.001); dysfunction (clara secretory [CC16], 0.001), (Cystatin C [p 0.001]; neutrophil gelatinase-associated lipocalin [NGAL], 0.001). Plasma reflective cell- not transient-AKI. No differences no-AKI. Conclusion Transient no-AKI little no differences, while group demonstrated stronger anomalies across domains contrast what been non-COVID-19-related markers associated trajectories. These findings suggest can induce robust contributes persistence AKI, largely mediated through inflammatory responses.