Our research explored the effects of Hyparrhenia hirta (H. hirta) against kidney impairment caused by nitrate. Experimentation was performed on rats separated in three groups. Sodium nitrate (NaNO₃) was supplied everyday by gavage to treated groups (400 mg/kg BW) either alone, or co-administered with methanolic extract of H. hirta (200 mg/kg bw). Nephrotoxicity caused by sodium nitrate was objectified by an increase in plasma and a reduction in urine concentrations of urea and creatinine, while uric acid level decreased in plasma and increased in urine when compared to controls. Our results showed also, a significant decrease in clearance of creatinine in NaNO₃-treated group. In addition, sodium nitrate produced oxidative stress in the kidney characterized by enhanced lipid peroxidation, reduced total glutathione level and catalase, superoxide dismutase and glutathione peroxidase activities. Sodium nitrate provoked fragmentation of DNA as reflected by smear and no formation of ladder. Renal damages were characterized histologically after nitrate treatment by degeneration of renal tubule cells and mononuclear cells infiltration. Co-administration of H. hirta improved biomarkers of kidney toxicity, malondialdehyde level, activities of antioxidant enzymes and histological damages. We concluded that H. hirta had a significant role in animal protection from nitrate-induced kidney dysfunction.

Key words: Adult rats, Hyparrhenia hirta, Lipid peroxidation, NaNO_3, Nephrotoxicity