Most people who have renal failure are thought to have it for no known reason. Lead and other heavy metals in drinking water are often the hidden source of many kidney problems. Consequently, this research aims to examine the impact of low viscosity sodium alginate (LvSA) on lead-induced nephrotoxicity. Lead (0.2% lead acetate in drinking water for 5 weeks) was administered to rats to induce nephrotoxicity, evaluated through histopathological alterations, elevated serum creatinine, blood urea nitrogen, urinary N-acetyl-β-D-glucosaminidase (NAG), proteinuria, Thiobarbituric acid reactive substances (TBARS), and a reduction in reduced glutathione levels. Lead acetate (LA) poisoning caused changes in serum creatinine, proteinuria, glomerular filtration rate (GFR), blood urea nitrogen (BUN), Thiobarbituric acid reactive substances (TBARS), urinary N-acetyl-β D glucosaminidase (NAG), kidney weight/body weight ratio (KW/BW %), and creatinine clearance that show kidney damage. Low viscosity sodium alginate (LvSA) treatment results in a significant reduction in serum creatinine, blood urea nitrogen (BUN), urinary N-acetyl-β-D-glucosaminidase (NAG), urinary protein, kidney weight/body weight ratio (KW/BW %), and thiobarbituric acid reactive substances (TBARS) levels, with an increase in glutathione (GSH), creatinine clearance, and glomerular filtration rate (GFR). Consequently, the findings indicate that LvSA considerably mitigated lead-induced nephrotoxicity.