In view of inconsistent reports on the association between chronic lead (Pb) exposure and renal injury markers (potential site of injury), the present systematic review explored their association by reviewing studies that investigated chronic Pb-exposed and those without obvious Pb exposure. Studies reporting blood Pb levels(BLL) and biomarkers of kidney injury [i.e. N-acetyl-β-D-glucosaminidase (NAG), Micro-Globulin(μG) and others] among chronic Pb-exposed and unexposed individuals were systematically searched from digital databases available until February 26, 2024. Preferred Reporting Items of Systematic Reviews and Meta-Analysis Guidelines were adhered to during the execution. Pooled effect size and heterogeneity were estimated using the random effect model and I2Studies reporting blood Pb levels(BLL) and biomarkers of kidney injury [i.e. N-acetyl-β-D-glucosaminidase (NAG), Micro-Globulin(μG) and others] among chronic Pb-exposed and unexposed individuals were systematically searched from digital databases available until February 26, 2024. Preferred Reporting Items of Systematic Reviews and Meta-Analysis Guidelines were adhered to during the execution. Pooled effect size and heterogeneity were estimated using the random effect model and I2. Pooled quantitative analysis revealed elevated BLL [25.64 (21.59–29.70) µg/dL] Pb-exposed group. The pooled analysis confirmed significantly higher urinary NAG [0.68(0.26–1.10) units], α1μG [3.82(0.96–6.68) mg/g creatinine] β 2μG [1.5(0.86–2.14) units and serum creatinine [0.03(0.00–0.05) mg/dL] levels in Pb-exposed group, with high heterogeneity. Current observations indicate the proximal tubular injury as the early and potential site of Pb-induced renal injury. Pb-exposed individuals experience proximal tubular injury (KIM-1, NAG) and dysfunction (β2μG, α1μG, Cystatin-C) prior to obvious clinical renal failure. Present observations should caution the policymakers towards drafting regulations for periodic screening with markers of renal injury and / or dysfunction among those chronically exposed to lead despite the certainty of evidence is very low.
Chronic Pb exposure is associated with proximal tubular injury i.e. ↑ KIM-1 & NAG, earlier to onset of clinical renal failure.
Pb exposure is associated with proximal tubular dysfunction i.e. ↑ β2μG, α1μG & Cystatin-C, prior to clinical renal failure.
Existing literature is primarily observational and highly heterogeneous carrying high risk of bias.
The quality of evidence from existing studies is low.
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