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Review
. 2025 May 18;26(10):4825.
doi: 10.3390/ijms26104825.

Biomarkers as Beacons: Illuminating Sepsis-Associated Hepato-Renal Injury

Maria-Antoanela Pasare  1   2 , Cristian Sorin Prepeliuc  1   3 , Maria Gabriela Grigoriu  2 , Ionela-Larisa Miftode  2   4 , Egidia Gabriela Miftode  2   4
Affiliations
Review

Biomarkers as Beacons: Illuminating Sepsis-Associated Hepato-Renal Injury

Maria-Antoanela Pasare et al. Int J Mol Sci. .

Abstract

Sepsis, defined as a dysregulated host response to infection, is one of the leading causes of mortality worldwide. It unleashes in the organism a cascade of molecules, cytokines, and proteins which leads to an inflammatory storm. If this response to infection is uncontrolled, any organ is susceptible to damage. Acute kidney injury (AKI) is one of the most frequent organ dysfunctions in septic patients, and while it can be reversible, its presence leads to a higher burden of morbidity and mortality. While serum creatinine is essential in evaluating kidney function, the pathophysiology of AKI is not completely elucidated, and a plethora of novel biomarkers have been studied in the hope of an early diagnosis and fast treatment. While the liver is not as affected by sepsis, it plays an important role as a guardian by providing acute-phase proteins, activating neutrophils, and controlling iron balance. Acute liver failure (ALF) could impair the organism's capacity to contain and eliminate pathogens. Some molecules have been associated with either AKI or ALF, although biomarkers specific for organ dysfunction are difficult to validate. The aim of this review is to understand the role of several molecules in the pathophysiology of sepsis and their clinical ability for diagnosing or predicting sepsis-induced hepato-renal dysfunction.

Keywords: IL-18; IL-27; acute kidney injury; acute liver failure; ferritin; hepcidin; sepsis.

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Conflict of interest statement

The authors declare no conflicts of interest.

Figures

Figure 1
Figure 1
Overview of sepsis pathophysiology. FasL: Fas Ligand; HMGB1: high-mobility group box-1; NK: natural killer; Th: T helper cells; TLR: Toll-like Receptor; Treg: Regulatory T cell. Created in BioRender. Pasare, A. (2025) https://BioRender.com/0fgjo31. Accessed on 1 May 2025.
Figure 2
Figure 2
Overview of SA-AKI pathophysiology. Created in BioRender. Pasare, A. (2025) https://BioRender.com/1f9k56c. Accessed on 11 May 2025.
Figure 3
Figure 3
Levels of biomarkers in septic patients with and without liver impairment. Created in BioRender. Pasare, A. (2025) https://BioRender.com/g7vqax2. Accessed on 11 May 2025.
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