Systematic Review: Histopathological Effects of Acute and Chronic Lead Exposure on Rat Kidneys

Introduction: Lead (Pb) is a ubiquitous environmental pollutant with significant nephrotoxic effects due to its bioaccumulation and interference with cellular metabolism. The kidneys are particularly vulnerable to lead-induced oxidative stress and inflammation, leading to structural damage.Methods: A systematic review was conducted following PRISMA guidelines. Articles focusing on lead-induced histopathological changes in rat kidneys published between 2016 and 2020 were retrieved from PubMed, ScienceDirect, Google Scholar, and Medline using specific keywords. Studies involving experimental lead exposure in rats, administered via oral or intraperitoneal routes, were included.Results and discussion: Eleven relevant studies were identified, with exposure durations from 7 days to 8 weeks and doses ranging from 5 to 300 mg/kg. Acute high-dose exposure mainly caused tubular epithelial karyomegaly, vacuolar degeneration, and tubular dilatation. Chronic or sub-chronic exposure resulted in glomerular shrinkage, tubular atrophy, interstitial fibrosis, inflammatory infiltration, and basement membrane disruption. Intraperitoneal administration produced more rapid and severe lesions compared to oral exposure. Lead nephrotoxicity severity correlates with dosage, exposure duration, and administration route. High oral doses of lead (300 mg/kgBW) or low intraperitoneal doses (8 mg/kgBW) induce kidney damage within 1–4 weeks. Moderate oral doses (20–40 mg/kgBW) cause renal injury after 4–8 weeks, while very low concentrations (0.25–3%) administered in drinking water (ad libitum) result in kidney damage after 8 weeks.Conclusion: Lead exposure induces dose-, time-, and route-dependent progressive kidney histopathological damage in rats. Understanding these parameters is vital for evaluating lead nephrotoxicity mechanisms and guiding preventive and therapeutic strategies.