Liang et al. lysosomal enzyme abundantly present in cells of renal proximal tubules, has a relatively high molecular weight of 130–140 kDa, which nor- mally precludes its filtration by the glomerular basal membrane (Kawada et al. 1989; Price 1992). Because of NAG’s direct relevance to the integrity of proximal tubular cells, the release of NAG into the urine is an early sign of tubular membrane damage (Bernard et al. 1995; Jin et al. 1999). In addition, our recent animal study (Liang et al. 2010) con- firmed increased hepatic and decreased uri- nary metallothioneins (a family of 6- to 7-kDa stress proteins incorporating a high content of cysteine and divalent metals) after cessation of oral Cd exposure, suggesting that urinary metallothionein could be another informative marker to evaluate recovery of Cd-mediated renal tubular dysfunction after a reduction in exposure. A previous smaller study carried out over 3 years (1995–1998) in the same popula- tion described here indicated reversibility of β2-microglobulin and albumin excretion for individuals with UCd < 10 μg/g creatinine and progression at higher UCd (Wu et al. 2008). In the present study, we observed no such progression for β2-microglobulin at UCd > 10 μg/g creatinine; for albumin, a recovery was evident regardless of UCd value. Although we did not consider the relationship to BCd in the earlier study (Wu et al. 2008), it can be assumed that the 3-year period was too short to allow a sufficient decrease in BCd and liver Cd and an inflow of metallothion- ein-bound Cd from the liver to the kidney. Conclusions Our findings suggest that a Cd-mediated increase in urinary albumin excretion (at the observed exposure levels) is a reversible effect that resolves after exposure is substantially reduced. 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