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The incidence of posterior urethral valves is estimated to be from 3:1000 to 8:1000 and this is one of the most common causes of obstruction of urinary tract in boys. About 13-17% of children with posterior urethral valves develop end stage renal failure. We present a  6-month-old boy with late diagnosis of posterior urtehral valves. Antenatal ultrasound investigation of the urinary tract was normal. A small degree of oligohydramnios was found during delivery. At the age of six months the boy was admitted to hospital because of urinary tract infection, hypertension (130/90 mmHg) and acute kidney injury (urea - 46 mg/dL, creatinine - 1.1 mg/dL, GFR - 35.5 mL/min/1.73 m2 ). Bilateral hydronephrosis and megaureters, low-capacity bladder with hypertrophied wall were seen on ultrasound examination. Voiding cystourethrograhy revealed vesicoureteral refluxes (III/V), hypertrophy of the bladder wall with numerous diverticula and dilated posterior urethra. During urethroscopy urethral valves were resected. Increased intravesical pressure (leak point up to 305 cm H2 O) was found on urodynamic test. Renal scintigraphy (99mTc-EC) revealed decreased intake of isotope in the left kidney (5%), and the right kidney intake was 95% ERPF. The patient was qualified for left-sided nephrectomy, which was postponed because of high leak point and high risk of worsening of vesicoureteral reflux to right kidney after nephrectomy. Anticholinergic and α-blocker treatment was started. At the age of 11 months left-side nephrectomy was performed because of recurrent urinary tract infections. After 3.5-year follow-up blood pressure, physical development, kidney function tests, and urinalysis are normal. Additionally to this investigation the significance of early diagnosis including prenatal (PUV) for further development as well as further therapeutic procedure is discussed.

Congenital chloride diarrhoea is a rare autosomal recessive disease and the diagnosis is frequently delayed. The disease is most common in Saudi Arabia and Kuwait 1:3200-13 000 births, Finland - 1:30 000-40 000, and in Poland - 1:200 000. Congenital chloride diarrhoea begins in fetal life. The main clinical sign is watery diarrhea that in utero leads to dilated bowel loops, polyhydramnios and often premature birth. Newborns have distended abdomens, absence of meconium, dilated bowel loops in ultrasonography and watery diarrhea which can sometimes be mistaken for urine. The absence of meconium and the distended abdomen suggest meconium ileus or Hirschsprung disease and can lead to unnecessary surgical intervention. The article is a report on a 3-months old boy with the history of dilated bowel loops in prenatal ultrasonograhy, low birth weight and abdominal distention. Because of the suspicion of mechanical bowel obstruction he had laparotomy on the second day of his life. Mechanical obstruction was excluded and enterostomy was performed. Hyponatremia, hypokaliemia and metabolic alkalosis were found in laboratory tests. The electrolyte disturbances were corrected and enterostomy was closed after six weeks. The final diagnosis of congenital chloride diarrhea was established two months later, when the patient was admitted to hospital again with severe watery diarrhea, metabolic alkalosis, hypochloraemia and hypokalemia. The stool chloride concentration was >90 mmol/L. Water and electrolyte deficits had been corrected. The patient was discharged home with supplementation of sodium, potassium and chloride. His follow-up was uneventful. He remains under the care of the pediatric clinic.

Unlabelled: The most common causes of laryngeal stridor are laryngomalacia (60%), vocal cord paralysis (VCP) (10 %) and subglottic laryngeal stenosis. Majority of cases of VCP are idiopathic, less frequently it is the effect of abnormalities in central nervous system (Arnold - Chiari syndrome, hydrocephalus, neonatal hypoxia). Differential diagnosis should also include anomalies of aortic arch and its branches (vascular rings). The authors present two cases of neonatal congenital laryngeal stridor. In the first case the girl presented with VCP of unknown etiology. The perinatal period was normal, ultrasound of central nervous system and neurologic examination revealed no abnormalities. Due to sustained VCP in control laryngeal ultrasound examinations, tracheostomy was performed in the third month of life. In the second case, stridor was caused by laryngomalacia and subglottic laryngeal stenosis of first grade according to Meyer-Cotton scale (larynx lumen diameter <4 mm). The diagnosis was established by laryngotracheobronchoscopy. In both children angiotomography was performed and vascular ring was diagnosed (aberrant right subclavian artery). Vascular anomaly was suspected in barium X-ray. In both cases echocardiographic examination did not visualize the fourth vessel of the aortic arch. Chest X- rays were normal. Both children had no symptoms caused by vascular ring., Conclusion: Diagnosis of congenital laryngeal stridor is an indication for complete evaluation to establish the cause of the airway obstruction. The differential diagnosis should include laryngomalacia, vocal cord paralysis, subglottic laryngeal stenosis, congenital anomalies of large vessels and abnormalities of the central nervous system.