Predictive factors for survival in patients with oligohydramnios secondary to antenatal kidney disease.


Journal

Pediatric nephrology (Berlin, Germany)
ISSN: 1432-198X
Titre abrégé: Pediatr Nephrol
Pays: Germany
ID NLM: 8708728

Informations de publication

Date de publication:
06 2023
Historique:
received: 09 05 2022
accepted: 24 10 2022
revised: 24 10 2022
medline: 4 5 2023
pubmed: 22 11 2022
entrez: 21 11 2022
Statut: ppublish

Résumé

Renal oligohydramnios (ROH) is caused by bilateral congenital abnormalities, either of renal parenchymal or obstructive origin. ROH is a poor prognostic factor of neonatal survival; lung hypoplasia is reported to be the main cause of mortality. We aimed to describe the fetal morbidity and pre- and postnatal mortality in case of ROH due to renal congenital pathologies and to find predictive risk factors for morbidity and mortality. All data were collected in Trousseau Hospital in the obstetric, neonatology, and pediatric nephrology units, from 2008 to 2020. We included 66 fetuses with renal parenchymal pathologies posterior urethral valves (PUV) (N = 25), bilateral kidney agenesis (N = 10), hypodysplasia (N = 16), and polycystic kidney disease (N = 10) causing oligohydramnios identified on antenatal ultrasound. Total pre- and postnatal mortality was 76% (50/66). Mortality, excepting termination of pregnancy (TOP), was 65%. The presence of pneumomediastinum and pneumothorax was not different in survivors and non-survivors. Fetuses with kidneys having features of hypodysplasia on ultrasound at T2 and those with oligohydramnios before 32 weeks GA had a higher risk of death. There was a significant difference in plasma creatinine of the surviving patients compared to the deceased patients, from day 3 onwards (183 µmol/L [88; 255] vs. 295 µmol/L [247; 326]; p = 0.038). The main differences between survivors and non-survivors among patients with "renal oligohydramnios" were oligohydramnios detection before 32 weeks GA, dysplasia detection on the second trimester ultrasound, and increase of serum creatinine from day 3 onwards. A higher resolution version of the Graphical abstract is available as Supplementary information.

Sections du résumé

BACKGROUND
Renal oligohydramnios (ROH) is caused by bilateral congenital abnormalities, either of renal parenchymal or obstructive origin. ROH is a poor prognostic factor of neonatal survival; lung hypoplasia is reported to be the main cause of mortality. We aimed to describe the fetal morbidity and pre- and postnatal mortality in case of ROH due to renal congenital pathologies and to find predictive risk factors for morbidity and mortality.
METHODS
All data were collected in Trousseau Hospital in the obstetric, neonatology, and pediatric nephrology units, from 2008 to 2020.
RESULTS
We included 66 fetuses with renal parenchymal pathologies posterior urethral valves (PUV) (N = 25), bilateral kidney agenesis (N = 10), hypodysplasia (N = 16), and polycystic kidney disease (N = 10) causing oligohydramnios identified on antenatal ultrasound. Total pre- and postnatal mortality was 76% (50/66). Mortality, excepting termination of pregnancy (TOP), was 65%. The presence of pneumomediastinum and pneumothorax was not different in survivors and non-survivors. Fetuses with kidneys having features of hypodysplasia on ultrasound at T2 and those with oligohydramnios before 32 weeks GA had a higher risk of death. There was a significant difference in plasma creatinine of the surviving patients compared to the deceased patients, from day 3 onwards (183 µmol/L [88; 255] vs. 295 µmol/L [247; 326]; p = 0.038).
CONCLUSIONS
The main differences between survivors and non-survivors among patients with "renal oligohydramnios" were oligohydramnios detection before 32 weeks GA, dysplasia detection on the second trimester ultrasound, and increase of serum creatinine from day 3 onwards. A higher resolution version of the Graphical abstract is available as Supplementary information.

Identifiants

pubmed: 36409365
doi: 10.1007/s00467-022-05800-1
pii: 10.1007/s00467-022-05800-1
doi:

Types de publication

Journal Article

Langues

eng

Sous-ensembles de citation

IM

Pagination

1783-1792

Informations de copyright

© 2022. The Author(s), under exclusive licence to International Pediatric Nephrology Association.

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Auteurs

Mathilde Baudin (M)

Pediatric Nephrology Unit, Trousseau Hospital- ORIGYNE- AP-HP.Sorbonne Université, Paris, France.

Claire Herbez (C)

Pediatric Nephrology Unit, Trousseau Hospital- ORIGYNE- AP-HP.Sorbonne Université, Paris, France.

Isabelle Guellec (I)

Pediatric Intensive Care Unit, Trousseau Hospital- ORIGYNE- AP-HP.Sorbonne Université, Paris, France.

Ferdinand Dhombres (F)

Fetal Medicine Department, Trousseau Hospital- ORIGYNE- AP-HP.Sorbonne Université, Paris, France.

Lucie Guilbaud (L)

Fetal Medicine Department, Trousseau Hospital- ORIGYNE- AP-HP.Sorbonne Université, Paris, France.

Cyrielle Parmentier (C)

Pediatric Nephrology Unit, Trousseau Hospital- ORIGYNE- AP-HP.Sorbonne Université, Paris, France.

Jean Daniel Delbet (JD)

Pediatric Nephrology Unit, Trousseau Hospital- ORIGYNE- AP-HP.Sorbonne Université, Paris, France.

Catherine Garel (C)

Radiology Department, Trousseau Hospital- AP-HP.Sorbonne Université, Paris, France.

Eleonore Bondiaux (E)

Radiology Department, Trousseau Hospital- AP-HP.Sorbonne Université, Paris, France.

Jean Marie Jouannic (JM)

Fetal Medicine Department, Trousseau Hospital- ORIGYNE- AP-HP.Sorbonne Université, Paris, France.

Tim Ulinski (T)

Pediatric Nephrology Unit, Trousseau Hospital- ORIGYNE- AP-HP.Sorbonne Université, Paris, France. tim.ulinski@aphp.fr.
Pediatric Nephrology, Trousseau Hospital- ORIGYNE- AP-HP.Sorbonne Université, 26 Av du Docteur Arnold Netter, Paris, 75012, France. tim.ulinski@aphp.fr.

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