Nickan Research Institute Journal of Renal Injury Prevention 2345-2781 15 2 2026 06 18 Protective effects of silymarin against favipiravir-induced renal injury in rats; a biochemical, histopathological, and immunohistochemical study e38718 e38718 10.34172/jrip.2026.38718 EN Bnar R. Abdalrahman https://orcid.org/0009-0000-2209-6355 Rebin Azad Omar https://orcid.org/0000-0002-0921-051X Harem Kh. Awla https://orcid.org/0000-0003-1725-1730 Azheen S. Abdulrahman https://orcid.org/0000-0001-8584-2458 Lana S. Saleh https://orcid.org/0000-0001-8698-8598 Khder H. Rasul https://orcid.org/0000-0002-5168-6802 Journal Article 10.34172/jrip.2026.38718 2025 11 07 2026 02 17 Introduction: Favipiravir, an antiviral agent widely used during the COVID-19 pandemic, has demonstrated therapeutic potential but has raised concerns regarding organ toxicity. Although its clinical benefits are well established, evidence of its nephrotoxic effects remains inconsistent. Objectives: This study aimed to evaluate the nephrotoxic effects of favipiravir and assess whether co-administration of silymarin could mitigate favipiravir-induced kidney injury. Materials and Methods: In this experimental study, 15 adult albino rats were randomly allocated into three groups (n = 5); group 1 received saline (control), group 2 was treated with favipiravir (1800 mg/kg on day one, followed by 800 mg/kg twice daily for 13 days), and group 3 received the same favipiravir regimen combined with silymarin (50 mg/kg twice daily). At the end of the 14-day treatment period, blood samples were collected to measure serum creatinine, blood urea, and blood urea nitrogen (BUN) levels. Kidneys were harvested for histopathological examination and immunohistochemical analysis using cytokeratin 7 (CK7) and paired box gene 8 (PAX8) markers. Results: No significant differences were observed in serum creatinine, blood urea, or BUN among the groups. However, histopathological analysis revealed glomerular atrophy, coagulative necrosis, lymphocytic infiltration, and interstitial hemorrhage in the kidneys of favipiravir-treated rats. These changes were less severe in rats treated with silymarin. Immunohistochemical staining showed strong CK7 and PAX8 expression in favipiravir-treated rats, whereas both markers were absent in control and silymarin-treated groups. Conclusion: Although favipiravir did not significantly alter kidney function parameters, histopathological findings indicate renal injury. The partial improvement observed in the silymarin-treated group suggests a potential nephroprotective effect, which warrants further investigation.