Pathogenesis, Biomarkers, and Therapeutic Prospects of Sepsis-Associated Acute Kidney Injury
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Keywords

Sepsis-associated acute kidney injury
Biomarkers
Pathogenesis
Inflammatory response
Pyroptosis

DOI

10.26689/ur.v3i4.13540

Submitted : 2025-12-13
Accepted : 2025-12-28
Published : 2026-01-12

Abstract

Sepsis-associated acute kidney injury (SA-AKI) is a common critical complication in the ICU, characterized by a complex pathogenesis involving the interplay of multiple factors such as inflammatory imbalance, vascular dysfunction, coagulation disorders, and cellular metabolic abnormalities. Traditional diagnostic indicators like serum creatinine and blood urea nitrogen exhibit lag time, making early identification challenging. In recent years, novel biomarkers have provided new directions for early diagnosis and risk stratification, including tubular injury markers (KIM-1, NGAL, L-FABP), renal function and glomerular injury markers (CysC, sCD35-uEV), cell cycle arrest markers ([TIMP-2] × [IGFBP7]), and inflammatory markers (IL-18, sTREM-1). Currently, supportive therapy remains the mainstay of treatment, encompassing early anti-infection measures, hemodynamic optimization, and timely renal replacement therapy. Novel therapeutic targets addressing the pathogenesis, such as regulating pyroptosis and improving mitochondrial dysfunction, are currently in preclinical and early clinical research stages, offering hope for future specific treatments.

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