Perinatal management of a preterm neonate affected by hyperprostaglandin E2 syndrome (HPS)

Background: Neonates affected by hyperprostaglandin E2 syndrome (HPS) present with severe polyuria. Both urinary losses as well as prostaglandin synthesis inhibitors may precipitate acute renal failure (ARF). Aim: Our goal was to maintain euvolaemia by replacement of urinary losses. Patient: Our pat...

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Bibliographic Details
Published in:Acta Pædiatrica 2005-11, Vol.94 (11), p.1690-1693
Main Authors: KÖMHOFF, MARTIN, TEKESIN, ISMAIL, PETERS, MELANIE, LEONHARD, ANDREAS, SEYBERTH, HANNSJÖRG W.
Format: Article
Language:English
Subjects:
Banter syndrome
Bartter Syndrome - therapy
Biological and medical sciences
Cyclooxygenase Inhibitors - therapeutic use
cyclooxygenase-2
Female
General aspects
Glomerulonephritis
Humans
Indomethacin - therapeutic use
Infant, Newborn
macula densa
Medical sciences
neonatal renal failure
Nephrology. Urinary tract diseases
Nephropathies. Renovascular diseases. Renal failure
Perinatal Care
Renal failure
Renal Insufficiency - prevention & control
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Summary:Background: Neonates affected by hyperprostaglandin E2 syndrome (HPS) present with severe polyuria. Both urinary losses as well as prostaglandin synthesis inhibitors may precipitate acute renal failure (ARF). Aim: Our goal was to maintain euvolaemia by replacement of urinary losses. Patient: Our patient was born prematurely with a family history typical of HPS. Urinary salt and water losses and PGE2 excretion were determined in 2‐ to 4‐h intervals. Salt and water were replaced accordingly. Results: Within the first 48 h, urinary losses and PGE2 increased continuously to 50 ml/kg/h and 374 ng/h/1.73 m2, respectively. Following exposure to 0.05–0.5 mg/kg/d indomethacin, urinary output decreased steadily to 10–15/ ml/kg/h. Conclusion: In euvolaemic preterm neonates with HPS and the need for excessive replacement of salt and water, inhibition of renal PGE2 excretion with indomethacin effectively reduces polyuria and natriuresis without acutely compromising renal function.
ISSN:0803-5253
1651-2227
DOI:10.1080/08035250510043897