Histopathological alterations in kidney tissue following experimental endotoxemia in a murine model

Vitaliy Antoniuk; Svitlana Pavlovych; Bogdan Dzhuran; Olena Kondratska; Roman Yanchii

doi:10.31450/ukrjnd.1(85).2025.07

Vitaliy Antoniuk Bogomoletz Institute of Physiology National Academy of Sciences of Ukraine, Kyiv, Ukraine https://orcid.org/0009-0009-7301-3594
Svitlana Pavlovych Bogomoletz Institute of Physiology National Academy of Sciences of Ukraine, Kyiv, Ukraine https://orcid.org/0000-0001-7946-6679
Bogdan Dzhuran Shupyk National Healthcare University of Ukraine, Kyiv, Ukraine https://orcid.org/0000-0003-3085-5862
Olena Kondratska Bogomoletz Institute of Physiology National Academy of Sciences of Ukraine, Kyiv, Ukraine https://orcid.org/0000-0002-3496-0603
Roman Yanchii Bogomoletz Institute of Physiology National Academy of Sciences of Ukraine, Kyiv, Ukraine https://orcid.org/0000-0001-7129-7698

DOI: https://doi.org/10.31450/ukrjnd.1(85).2025.07

Keywords: lipopolysaccharides, endotoxemia, acute kidney injury, mice, histological techniques.

Abstract

Acute kidney injury (AKI) is a clinical syndrome characterized by a rapid decline in kidney function and represents a serious threat to human health. One of the most common causes of AKI is endotoxemia or sepsis, triggered by the hyperactivation of the immune system in response to gram-negative bacterial infections. The pathogenesis of AKI is highly complex and not yet fully understood. The present study aimed to investigate histostructural changes in kidney tissue using a model of inflammation induced by lipopolysaccharide (LPS), a key component of the outer membrane of gram-negative bacteria.

Methods. Systemic endotoxemia was induced in mice by intraperitoneal injection of LPS (E. coli O111:B4, Sigma, USA) at a dose of 3 mg/kg body weight. Control animals received saline injections. After 24 hours, the animals were anesthetized with ether, and kidney tissue samples were collected for analysis. For histological evaluation, kidney tissue specimens were fixed in 10% neutral formalin, processed using standard histological techniques, embedded in paraffin, sectioned, stained with hematoxylin-eosin, and examined under a light microscope.

Results. LPS injection resulted in pronounced neutrophilia in the blood leukogram: the percentage of rod-shaped neutrophils increased 3.6-fold while the percentage of segmented neutrophils increased 2.7-fold (p < 0.05), which indicates systemic inflammatory response. Significant histostructural damage to kidney tissue was detected under these conditions. Dystrophic and necrotic changes were observed in Bowman's capsules. Circulatory disturbances were evident, with morphological alterations in all layers of the vascular walls and destruction of the epithelium in the proximal and distal convoluted tubules.

Conclusions. The findings indicate that systemic inflammation induced by LPS leads to substantial morphological alterations in kidney tissue. These changes include circulatory disturbances, structural damage to vascular glomeruli, and epithelial injury in the proximal and distal convoluted tubules. The observed damage results in a reduction in the number of functioning nephrons, which may contribute to the progression of kidney failure.