Velibor Tasic1, Liljana Pota, Zoran Gucev. 1. Department of Pediatric Nephrology, University Children's Hospital, Skopje, Macedonia. vtasic2003@gmail.com
Abstract
BACKGROUND: antenatal variant of Bartter syndrome is characterized by a history of polyhydramnios, premature birth, metabolic alkalosis, hypokalemia, polyuria and renal salt wasting. In this report we present a premature female baby with antenatal Barter syndrome who had three episodes of urinary tract infection (UTI), without evidence for congenital anomaly of the kidneys or urinary tract. METHODS: antenatal Bartter syndrome was diagnosed according to the standard criteria. Ultrasound scan and voiding cystourethrography were performed to exclude congenital anomaly of the kidneys and urinary tract. RESULTS: the baby presented with early hyperkalemia and acidosis. The typical biochemical features of the Bartter syndrome were observed in the second month. Despite appropriate treatment she had persistent hypercalciuria. The clinical course was complicated with recurrent episodes of febrile UTIs. Urinary tract system imaging did not demonstrate congenital anomalies. She finally died of severe dehydration, acidosis and renal failure. CONCLUSION: since no congenital anomaly of the kidneys or urinary tract was demonstrated in our patient, we believe that severe, persistent hypercalciuria is the most important risk factor for development of recurrent UTIs.
BACKGROUND: antenatal variant of Bartter syndrome is characterized by a history of polyhydramnios, premature birth, metabolic alkalosis, hypokalemia, polyuria and renal salt wasting. In this report we present a premature female baby with antenatal Barter syndrome who had three episodes of urinary tract infection (UTI), without evidence for congenital anomaly of the kidneys or urinary tract. METHODS: antenatal Bartter syndrome was diagnosed according to the standard criteria. Ultrasound scan and voiding cystourethrography were performed to exclude congenital anomaly of the kidneys and urinary tract. RESULTS: the baby presented with early hyperkalemia and acidosis. The typical biochemical features of the Bartter syndrome were observed in the second month. Despite appropriate treatment she had persistent hypercalciuria. The clinical course was complicated with recurrent episodes of febrile UTIs. Urinary tract system imaging did not demonstrate congenital anomalies. She finally died of severe dehydration, acidosis and renal failure. CONCLUSION: since no congenital anomaly of the kidneys or urinary tract was demonstrated in our patient, we believe that severe, persistent hypercalciuria is the most important risk factor for development of recurrent UTIs.
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