Nephrotoxic Effects of Varying Lead Acetate Doses on Kidney Biochemical Markers and Histology in Adult Male Rats.

Background: Lead is a non-essential, persistent environmental toxicant with no known beneficial biological role, and the kidney remains one of its principal target organs. Despite decades of research, the relationship between oral lead acetate dose and the magnitude of renal biochemical and structural injury continues to be refined. Objective: This study evaluated the dose-dependent effects of orally administered lead acetate on serum renal function biomarkers and kidney histoarchitecture in adult male Wistar rats. Methods: Twenty adult male Wistar rats (150–200 g) were randomly allocated into four groups (n = 5): a distilled-water control and three treatment groups receiving lead acetate at 100, 200, or 400 mg/kg body weight by oral gavage daily for 21 days. Serum urea, creatinine, and uric acid were assayed, and kidney sections were processed for haematoxylin and eosin (H&E) histology. Data were analysed by one-way ANOVA with Duncan’s Multiple Range Test (p < 0.05). Results: Serum urea and creatinine were numerically highest in the 400 mg/kg group, consistent with a decline in glomerular filtration rate at high-dose exposure, while the 200 mg/kg group showed comparatively modest deviation from control. Serum uric acid was significantly elevated in both the 100 mg/kg and 400 mg/kg groups relative to control, indicating that renal stress was detectable even at the lowest dose tested. Histopathology revealed a clear dose-dependent gradient, progressing from preserved glomerular and tubular architecture in the control group to mild glomerular shrinkage and tubular dilation at 100 mg/kg, moderate glomerular collapse with inflammatory infiltration at 200 mg/kg, and severe glomerular distortion, haemorrhage, and extensive interstitial inflammation at 400 mg/kg. Conclusion: Subacute oral lead acetate exposure produces dose-dependent biochemical and morphological nephrotoxicity in Wistar rats, with serum uric acid emerging as a sensitive early indicator of renal injury that precedes overt elevation of urea and creatinine. These findings reinforce the need for renal biomonitoring in lead-exposed populations and support continued evaluation of nephroprotective strategies.

Lead acetate; nephrotoxicity; Wistar rats; renal biomarkers

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