Azotemia is associated with the use of decadron in infants being treated for bronchopulmonary dysplasia. The purpose of this study was to further characterize the azotemia reported in infants treated with steroids for BPD. We retrospectively examined twenty charts of infants who received at least a seven day course of decadron for the treatment of BPD. Infants who received decadron were matched for gestational age, weight and postnatal age with infants who did not receive decadron. Electrolytes, BUN and Creatinine levels were examined daily from one day prior to treatment (D0) through the seventh day. Daily intake and urine outputs were also examined. The mean±SD BW and GA were 819±274g and 26±2wks for the treated group compared to 820±247g and 26±2wk for the untreated group (p=NS). By Student t-test, BUN (mg/dl) was significantly elevated in the treated group from day one of treatment through day seven. Creatinine levels (mg/dl) were also elevated in the treated group compared to the untreated group on day 2(1.2±0.4 vs. 0.8±0.4) and on day 3 (1.2±0.5 vs. 0.8±0.3), p=0.02 for both comparison. There were no differences with respect to fluid intake, total caloric intake or protein intake. There was an increase in urine output in the decadron group on days 1, 3, 4 and 6 which may be explained by the hyperglycemia noted in some of the infants who were given decadron. These data show that the elevation in BUN associated with the use of decadron in neonates for the treatment of BPD is not related to a decrease in urine output and presumably not associated with an impaired GFR. We speculate that in the abscence of a renal etiology for an elevated BUN, the azotemia associated with the use of steroids in the treatment of BPD is due to increased catabolism. Table

Table 1
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