DOI: 10.12688/f1000research.182793.2 ISSN: 2046-1402

Early Identification of Sepsis-induced Acute Kidney Injury Utilizing NGAL, Cystatin C, Urine Output, and Serum Creatinine in a Porcine (Sus scrofa) Model of Septic Shock: A comparative Study of Fluid and Vasopressor Strategies

Andriamuri Primaputra Lubis, Syah Mirsya Warli, Tasrif Hamdi, Gunanti Gunanti, Antonius Hocky Pudjiadi, Muhammad Rusda, Cut Meliza Zainumi, Raka Jati Prasetya
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Background Sepsis-associated acute kidney injury (SA-AKI) contributes significantly to ICU morbidity and mortality, yet early detection remains challenging due to the delayed response of conventional markers such as serum creatinine and urine output. This study aimed to evaluate the temporal patterns of early renal biomarkers—neutrophil gelatinase-associated lipocalin (NGAL) and cystatin C—compared with conventional functional markers in a porcine model of septic shock under three fluid and vasopressor resuscitation strategies. Methods In a randomized experimental study, six Sus scrofa pigs underwent standardized septic shock induction and were allocated into three resuscitation groups: Ringer’s lactate (30 mL/kg), fluid combined with early norepinephrine infusion, or early norepinephrine with maintenance fluids. Plasma NGAL, cystatin C, serum creatinine, and ultrasonographically assessed urine dynamics were measured sequentially alongside continuous hemodynamic monitoring. Data were analyzed using repeated-measures and nonparametric tests (p < 0.05). Results NGAL and cystatin C exhibited numerical temporal fluctuations across observation periods and differing trajectories among resuscitation strategies. Post-intervention decreases in NGAL and cystatin C coccurred in fluid-based groups, whereas early norepinephrine administration was followed by numerical increases. However, neither between-group nor within-group temporal changes reached statistical significance for NGAL, cystatin C, or serum creatinine. Conclusion In this exploratory pilot study, NGAL and cystatin C displayed numerical temporal shifts during septic shock; however, these changes lacked statistical significance and cannot establish early SA-AKI detection. Given the unstandardized urine output criteria and non-significant creatinine kinetics, these findings represent exploratory evidence of renal biomarker dynamics rather than definitive diagnostic proof of SA-AKI.

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