Abstract
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.