In the adult rat, it has been shown that chronic cadmium intoxication induces nephropathy with Fanconi-like features. This result raises the question of whether intoxication of pregnant rats has any deleterious effect on renal function in their offsring. To test this hypothesis, we measured the renal function of 2 to 60 days postnatal offspring from female rats administered cadmium chloride by the oral route (0.5 mg/kg/day) throughout their entire gestation. The investigations of rats from contaminated pregnant rats show the presence of cadmium in the kidney at gestational day 20 (GD20). After birth, cadmium kidney concentration increases from postnatal day 2 to 60 (PND2 to 60), presumably due first to milk contamination and second to neonatal liver cadmium content release. Although the renal parameters (glomerular filtration, U/P inulin, and urinary excretion rate) are not significantly affected until PND45, renal failure appeared at PND60, as demonstrated by a dramatical decrease of the glomerular filtration rate associated with an increase of the excretion of the main ions. In parallel, immunofluorescence study of tight junction protein expression of PND60 offspring from contaminated rats has shown a disorganisation of tight-junction proteins claudin-2 and claudin-5, specifically expressed in the proximal tubule and glomerule, respectively. In contrast, the expression of a distal claudin protein, claudin-3, is not affected. In conclusion, in utero exposure of cadmium leads to a toxic renal effect in adult offspring. This results suggests that the contamination of pregnant rats represents a serious and critical hazard for the renal function of their offpsring.