{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2025,9,25]],"date-time":"2025-09-25T13:44:04Z","timestamp":1758807844792,"version":"3.44.0"},"reference-count":11,"publisher":"BMJ","issue":"4","content-domain":{"domain":["bmj.com"],"crossmark-restriction":true},"short-container-title":["BMJ Case Rep"],"accepted":{"date-parts":[[2021,3,19]]},"published-print":{"date-parts":[[2021,4]]},"abstract":"<jats:p>Bartter syndrome (BS) is a well-recognised inherited tubular dysfunction that causes polyuria, metabolic alkalosis and hypokalaemia. Among BS cases, antenatal\/neonatal BS (ABS) usually shows distinct polyhydramnios prenatally and presents features of BS in the early neonatal period. We encountered a premature infant with type 3 ABS presenting with mild polyuria and discuss the pathogenesis of mild polyuria in type 3 ABS. A male infant was born at 31 weeks\u2019 gestation. His mother received amniocentesis because of polyhydramnios. Hyponatraemia and hypokalaemia appeared within 3 days after birth. Metabolic alkalosis, hyperreninaemia and hyperaldosteronism were also identified. Temporary polyuria developed at 1 month after birth; however, the mean urine output during hospitalisation was within the normal range. <jats:italic>CLCNKB<\/jats:italic> compound heterozygous mutations were confirmed. Polyuria of type 3 ABS may be less severe than in other types of ABS. Lower urine sodium loss may be a characteristic feature of type 3 ABS.<\/jats:p>","DOI":"10.1136\/bcr-2021-242086","type":"journal-article","created":{"date-parts":[[2021,4,7]],"date-time":"2021-04-07T14:27:00Z","timestamp":1617805620000},"page":"e242086","update-policy":"https:\/\/doi.org\/10.1136\/crossmarkpolicy","source":"Crossref","is-referenced-by-count":3,"title":["Type 3 antenatal Bartter syndrome presenting with mild polyuria"],"prefix":"10.1136","volume":"14","author":[{"ORCID":"https:\/\/orcid.org\/0000-0001-8184-6873","authenticated-orcid":false,"given":"Yuto","family":"Otsubo","sequence":"first","affiliation":[{"name":"Department of Pediatrics, Dokkyo Medical University, Shimotsuga-gun, Tochigi, Japan"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Yuji","family":"Kano","sequence":"additional","affiliation":[{"name":"Department of Pediatrics, Dokkyo Medical University, Shimotsuga-gun, Tochigi, Japan"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Hiroshi","family":"Suzumura","sequence":"additional","affiliation":[{"name":"Department of Pediatrics, Dokkyo Medical University, Shimotsuga-gun, Tochigi, Japan"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Shigemi","family":"Yoshihara","sequence":"additional","affiliation":[{"name":"Department of Pediatrics, Dokkyo Medical University, Shimotsuga-gun, Tochigi, Japan"}],"role":[{"role":"author","vocabulary":"crossref"}]}],"member":"239","published-online":{"date-parts":[[2021,4,7]]},"reference":[{"key":"2025082803345957000_14.4.e242086.1","doi-asserted-by":"crossref","first-page":"428","DOI":"10.1111\/ped.14089","article-title":"Inherited salt-losing tubulopathy: an old condition but a new category of tubulopathy","volume":"62","author":"Nozu","year":"2020","journal-title":"Pediatr Int"},{"key":"2025082803345957000_14.4.e242086.2","doi-asserted-by":"publisher","DOI":"10.1007\/s12519-015-0016-4"},{"key":"2025082803345957000_14.4.e242086.3","unstructured":"Modi N . 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