# Hypovitaminosis D Does Not Aggravate the Progression of Gentamicin-Induced Kidney Injury in Rats

**Authors:** Ana Lívia D. Maciel, Amanda L. Deluque, Beatriz M. Oliveira, Cláudia S. Souza, Heloísa D. C. Francescato, Cleonice Giovanini, Francisco J. A. de Paula, Terezila M. Coimbra, Rildo A. Volpini

PMC · DOI: 10.3390/diseases13070200 · 2025-06-28

## TL;DR

This study found that low vitamin D levels do not worsen kidney damage caused by gentamicin in rats.

## Contribution

The study is the first to show that hypovitaminosis D does not exacerbate gentamicin-induced kidney injury in rats.

## Key findings

- Gentamicin caused impaired renal function and structural damage in rats.
- Hypovitaminosis D did not worsen the kidney injury caused by gentamicin.
- Gentamicin increased inflammation and fibrosis markers in the kidneys.

## Abstract

Background/Objectives: Gentamicin is one of the most effective and widely used antibiotics to treat serious infections. In addition to its bactericidal properties, gentamicin has a nephrotoxic effect that results in acute kidney injury (AKI). AKI may be intensified by hypovitaminosis D. This study evaluated the effect of hypovitaminosis D in the progression of gentamicin-induced renal injury. Methods: Male Wistar Hannover rats received a standard (SD) or a vitamin D-free diet (VitD—) before gentamicin treatment. After that, we divided the animals into four groups: Ctrl VitD, SD diet, and saline injection; Ctrl VitD—, VitD— diet, and saline injection; Genta VitD, SD diet, and gentamicin injection (40 mg/kg; IM); Genta VitD—, VitD— diet, and gentamicin injection (40 mg/kg; IM). After the end of gentamicin treatment, we followed the animals for 5 days (protocol 1) and 30 days (protocol 2). Results: The Genta VitD group (protocol 1) presented impaired renal function. Regarding morphological analyses, the Genta VitD group presented necrotic tubules (protocol 1) and atrophied tubules (protocol 2). In the inflammatory scenario, the Genta VitD group presented an increase in the number of CD68+ cells, as well as in the levels of interleukin 1β (protocols 1 and 2). In addition, gentamicin-treated animals (protocols 1 and 2) presented an increased renal expression of vimentin and fibronectin. Despite the notable changes in functional, inflammatory, and structural parameters induced by gentamicin, hypovitaminosis D did not aggravate the renal injury in this experimental model. Conclusion: Hypovitaminosis D did not aggravate the progression of gentamicin-induced renal injury in rats.

## Linked entities

- **Proteins:** PRELID1 (PRELI domain containing 1), fn1.S (fibronectin 1 S homeolog), CD68 (CD68 molecule)
- **Chemicals:** gentamicin (PubChem CID 3467)
- **Diseases:** acute kidney injury (MONDO:0002492)
- **Species:** Rattus norvegicus (taxon 10116)

## Full-text entities

- **Genes:** Il1b (interleukin 1 beta) [NCBI Gene 24494] {aka IL-1F2}, Cd68 (Cd68 molecule) [NCBI Gene 287435], Vim (vimentin) [NCBI Gene 81818], Fn1 (fibronectin 1) [NCBI Gene 25661] {aka FIBNEC, fn-1}
- **Diseases:** AKI (MESH:D058186), necrotic (MESH:D009336), Kidney Injury (MESH:D007674), Hypovitaminosis D (MESH:D014808), infections (MESH:D007239), inflammatory (MESH:D007249)
- **Chemicals:** Genta VitD (-), VitD (MESH:D014807), Gentamicin (MESH:D005839)
- **Species:** Rattus norvegicus (brown rat, species) [taxon 10116]

## Figures

6 figures with captions in the complete paper: https://tomesphere.com/paper/PMC12293155/full.md

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Source: https://tomesphere.com/paper/PMC12293155