2 ± 0.1 mg/kg/d,ym divided in two doses, despite we have tried in 6; one patient presented severe hypotension and the drug was withdrawn. No significant changes were observed in height-for-age Z-score (median at the beginning

of treatment = -2.5 [-4.3 to -2.2]; median at the end = -3.0 [-3.9 to -1.21]; p = 0.8), nor in the weight-for-age Z-score (median at the beginning of treatment = -2.1 [-2.7 to -0.9]; median at the end= -2.7 [-3.8 to -0.3]; p = 0.4). The creatinine clearance showed no statistically significant differences, from median 150 (107-183) to 138 (62-160) (p = 0.18); however, a decrease was observed in four patients, one of whom below Protease Inhibitor Library cell line 90 mL/min/1.73m2BS. In this case, the dose of enalapril was reduced. Fig. 1 presents the weight-for-age Z-score, Fig. 2 shows the height-for-age Z-score at the beginning and at the end of the treatment with each drug. Fig. 3 presents the creatinine clearance during the treatment AZD6244 molecular weight with each drug. Seven patients developed microalbuminuria during treatment

with indomethacin; in five patients, the problem resolved when their treatment was converted to celecoxib; however, four patients developed microalbuminuria during the use of celecoxib. Patients with proteinuria had their treatment converted to ACEi, and presented a significant reduction: median was 76.2% (62.8%-80.6%). Table 1 presents the average of serum potassium, sodium, and bicarbonate levels of patients during each drug and the amount of potassium supplementation including data from each six months. No significant differences

were observed in serum potassium, sodium, and bicarbonate levels during the use of the three drugs. No significant differences were observed between the amount of potassium supplementation during the use of indomethacin and celecoxib (p = 0.8). Although no significant differences were detected in the amount of potassium supplementation during indomethacin and ACEi (p = 0.09) and celecoxib and ACEi (p = 0.2), a tendency to supplement a larger amount of potassium during ACEi was observed, as seen in Table 1. In BS, an over activation of renin-angiotensin-aldosterone system (RAAS) and an over production of PGs can be observed. Those findings are Oxymatrine the result of sodium, chloride, and potassium urinary wasting. Therefore, the recommended treatment has been based on potassium supplementation, a PGs inhibitor;7 and 8 spironolactone1 is also an option, but with transient effect, and ACEi has been used in some studies.9 Indomethacin has been long employed in the treatment of these patients. Studies have demonstrated that with indomethacin, spironolactone, and potassium chloride supplementation and, sometimes, sodium chloride supplementation, patients experience improvement in growth speed, weight gain, and metabolic stability.10 However, there are significant GI effects resulting from inhibition of cyclooxygenase (Cox) 1.