The effects of maternal exposure to glucocorticoids on various organ and systems including the kidney of the offspring have been reported in literature. The hallmark of this effect is an increase in circulating corticosterone. Excess corticosterone may also induce oxidative stress. This study examined the effects of maternal dexamethasone(dex) exposure on serum creatinine and urea, oxidative stress markers in the kidney and kidney architecture in the offspring. Pregnant rat (180-200g) were divided into 4 groups. Group 1 was administered 0.02ml/100gbwt/day normal saline through postnatal (PN) day 1-21 (control). Groups 2, 3, and 4 were administered 100µg/kg bwt/day dex for PN day 1-7 (Dex1-7),1-14( Dex 1-14), and 1-21(Dex 1-21) respectively. All administration was done subcutaneously. At 12weeks, male offspring were sacrificed. Evaluation of serum analyte, kidney oxidative stress and kidney histology were done. Level of lipid peroxidation (MDA) (Buege and Aust,1978), Catalase activity (Sinah,1971), SOD (Mistra and Fridovich 1972) activity, Protein (Lowrey et al 1951) were evaluated. Serum creatinine and Urea was estimated using analytical kit (Randox lab. USA). Tissue histology (H/E techniques). Values (Mean±SEM, n=6) are compared using one way ANOVA. P<0.05 is significant. Serum creatinine was Higher in the Dex1-7(0.234±0.018mg/dl), Dex1-14(0.254±0.019mg/dl) and Dex1-21(0.293±0.0195mg/dl) when compared with the control(0.140±0.016mg/dl) (P<0.01, 0.01, 0.001 respectively). Serum Urea level was higher in the treatment groups Dex1-7(6.995±0.44 mg/dl), Dex1-14 (4.232±0.898 mg/dl), Dex1-21(3.163±0.662) when compared with control (0.555±0.166) (P<0.001,0.01,0.05 respectively). However, serum urea level was higher in the Dex1-7 when compared with Dex1-14 and Dex1-21 (P<0.05,0.01 respectively) . Kidney MDA was also increase in the Dex1-7(11.525±0.813 mole/gtissue), Dex1-14(15.95±0.92 mole/gtissue) and Dex1-21(17.213± 1.09 mole/g tissue) groups compared to control(5.813±0.166 mole/g tissue)(P<0.01, 0.001, 0.001 respectively). However, kidney SOD and catalase activities in the treatment groups (Dex1-7 SOD-2.797±0.12 U/mg/ml protein, Cat-0.95±0.030Katf; Dex1-14 SOD-1.312±0.034 U/mg/mlprotein,Cat-0.765±0.03; Dex1-21 SOD-1.292±0.03 U/mg/mlprotein,Cat-0.404±0.0212) were all lower than the control (SOD-4.776±0.131U/mg/mlprotein,Cat-1.298±0.0845,)(P<0.001). Kidney protein was lower in the Dex 1-7(4.65±0.98 mg/ml), Dex1-14(4.21±0.24mg/ml), Dex1-21(3.29±0.94mg/ml) when compared with the control(6.98±0.04 mg/ml) (P<0.05,0.01,0.001 respectively). Histology of the kidney showed mild, moderate and severe tubular necrosis in the Dex1-7, Dex1-14, Dex1-21 group respectively. Results suggest that exposure to dex during lactation could lead to increase oxidative stress in the kidney and increase renal necrosis.