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A 3-day-old term, male infant presented to the emergency department for evaluation of bloody stools. The infant was born after an uncomplicated pregnancy followed by a normal spontaneous vaginal delivery. The mother was group B Streptococcus colonized, and received antenatal penicillin prophylaxis. The infant received routine delivery room care, and was given ophthalmic erythromycin and intramuscular vitamin K. Circumcision was performed without bleeding and he was discharged from the newborn nursery and the hospital after 48 hours. On the day of presentation, he had streaky bright red blood in 4 consecutive stools. After discussion with the infant’s pediatrician, the parents took him to the emergency department. The infant was afebrile, nursing well without emesis, and had made ∼10 wet diapers that day. The physical examination revealed a fussy infant with mild tachycardia, tachypnea, and scleral icterus. The complete blood count was unremarkable. Serum total bilirubin was 11.9 mg/dL, sodium 156 mmol/L, chloride 120 mmol/L, potassium 4.7 mmol/L, and bicarbonate 16 mmol/L. International normalized ratio was prolonged at 2.7, prothrombin time 26.6 seconds, partial thromboplastin time 38.9 seconds. The stool was hemeoccult positive. An obstructive radiograph series of the abdomen showed a nonobstructed gas pattern. Official radiology interpretation the following day reported possible pneumatosis intestinalis in the left and right colon. Our multidisciplinary panel will discuss the assessment of bloody stools in the term newborn, evaluation of electrolyte abnormalities, the diagnosis, and patient management.

This 4‐week randomized, double blind, placebo‐controlled study (N=240), 1‐year open label trial (N=233), and single‐dose pharmacokinetic study (N=22) evaluated candesartan cilexetil (3 doses) in hypertensive children aged 6 to 17 years. Seventy‐one percent were 12 years of age or older, 71% were male, and 47% were black. Systolic (SBP)/diastolic (DBP) blood pressure declined 8.6/4.8–11.2/8.0 mm Hg with candesartan and 3.7/1.8 mm Hg with placebo (P.05). The response rate (SBP and DBP

Late-preterm twins with propionic acidemia developed severe hyperammonemic encephalopathy at 5 days of age. Continuous venovenous hemodialysis was performed successfully for both infants via extracorporeal membrane oxygenation pump, and both rapidly improved. They were taken off continuous venovenous hemodialysis and extracorporeal membrane oxygenation and discharged with dietary therapy. At 3 years of age, neurodevelopment showed globally delayed milestones.

Brief periods of in vitro hypoxia/ischemia induce apoptosis of cultured renal epithelial cells, but the underlying mechanisms remain unknown. We show that partial ATP depletion (≈10–65% of control) results in a duration-dependent induction of apoptosis in Madin-Darby canine kidney (MDCK) cells, as evidenced by internucleosomal DNA cleavage (DNA laddering and in situ nick end labeling), morphological changes (cell shrinkage), and plasma membrane alterations (externalization of phosphatidylserine). The ATP-depleted cells display a significant upregulation of Fas, Fas ligand, and the Fas-associating protein with death domain (FADD). Exogenous application of stimulatory Fas monoclonal antibodies also induces apoptosis in nonischemic MDCK cells, indicating that they retain Fas-dependent pathways of programmed cell death. Furthermore, cleavage of poly(ADP)ribose polymerase (PARP) is evident after ATP depletion, indicating activation of caspases. Indeed, the apoptotic cells display a significant increase in caspase-8 (FLICE) activity. Finally, apoptosis induced by ATP depletion is ameliorated by pretreatment with inhibitors of caspase-8 (IETD), caspase-1 (YVAD), or caspase-3 (DEVD) but is not affected by inhibitors of serine proteases (TPCK). Our results indicate that partial ATP depletion of MDCK cells results in apoptosis and that Fas- and caspase-mediated pathways may play a critical role.