Longitudinal kidney injury biomarker trajectories in children with obstructive uropathy.


Journal

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

Informations de publication

Date de publication:
10 2020
Historique:
received: 20 03 2020
accepted: 05 05 2020
revised: 01 05 2020
pubmed: 24 5 2020
medline: 3 7 2021
entrez: 24 5 2020
Statut: ppublish

Résumé

Congenital obstructive uropathy (OU) is a leading cause of pediatric kidney failure, representing a unique mechanism of injury, in part from renal tubular stretch and ischemia. Tubular injury biomarkers have potential to improve OU-specific risk stratification. Patients with OU were identified in the Chronic Kidney Disease in Children (CKiD) study. "Cases" were defined as individuals receiving any kidney replacement therapy (KRT), while "controls" were age- and time-on-study matched and KRT free at last study visit. Urine and plasma neutrophil gelatinase-associated lipocalin (NGAL), interleukin 18 (IL-18), and liver-type fatty acid-binding protein (L-FABP) levels were measured at enrollment and annually and compared between cases and controls. Urine values were normalized to urine creatinine. In total, 22 cases and 22 controls were identified, with median (interquartile range) ages of 10.5 (9.0-13.0) and 15.9 (13.9-16.9) years at baseline and outcome, respectively. At enrollment there were no differences noted between cases and controls for any urine (u) or plasma (p) biomarker measured. However, the mean pNGAL and uL-FABP/creatinine increased throughout the study period in cases (15.38 ng/ml per year and 0.20 ng/ml per mg/dl per year, respectively, p = 0.01 for both) but remained stable in controls. This remained constant after controlling for baseline glomerular filtration rate (GFR). In children with OU, pNGAL and uL-FABP levels increased over the 5 years preceding KRT; independent of baseline GFR. Future studies are necessary to identify optimal cutoff values and to determine if these markers outperform current clinical predictors.

Sections du résumé

BACKGROUND
Congenital obstructive uropathy (OU) is a leading cause of pediatric kidney failure, representing a unique mechanism of injury, in part from renal tubular stretch and ischemia. Tubular injury biomarkers have potential to improve OU-specific risk stratification.
METHODS
Patients with OU were identified in the Chronic Kidney Disease in Children (CKiD) study. "Cases" were defined as individuals receiving any kidney replacement therapy (KRT), while "controls" were age- and time-on-study matched and KRT free at last study visit. Urine and plasma neutrophil gelatinase-associated lipocalin (NGAL), interleukin 18 (IL-18), and liver-type fatty acid-binding protein (L-FABP) levels were measured at enrollment and annually and compared between cases and controls. Urine values were normalized to urine creatinine.
RESULTS
In total, 22 cases and 22 controls were identified, with median (interquartile range) ages of 10.5 (9.0-13.0) and 15.9 (13.9-16.9) years at baseline and outcome, respectively. At enrollment there were no differences noted between cases and controls for any urine (u) or plasma (p) biomarker measured. However, the mean pNGAL and uL-FABP/creatinine increased throughout the study period in cases (15.38 ng/ml per year and 0.20 ng/ml per mg/dl per year, respectively, p = 0.01 for both) but remained stable in controls. This remained constant after controlling for baseline glomerular filtration rate (GFR).
CONCLUSIONS
In children with OU, pNGAL and uL-FABP levels increased over the 5 years preceding KRT; independent of baseline GFR. Future studies are necessary to identify optimal cutoff values and to determine if these markers outperform current clinical predictors.

Identifiants

pubmed: 32444926
doi: 10.1007/s00467-020-04602-7
pii: 10.1007/s00467-020-04602-7
pmc: PMC7502482
mid: NIHMS1598226
doi:

Substances chimiques

Biomarkers 0
FABP1 protein, human 0
Fatty Acid-Binding Proteins 0
IL18 protein, human 0
Interleukin-18 0
LCN2 protein, human 0
Lipocalin-2 0
Creatinine AYI8EX34EU

Types de publication

Journal Article Observational Study Research Support, N.I.H., Extramural

Langues

eng

Sous-ensembles de citation

IM

Pagination

1907-1914

Subventions

Organisme : NIDDK NIH HHS
ID : U01 DK066143
Pays : United States
Organisme : NIDDK NIH HHS
ID : U01 DK066174
Pays : United States
Organisme : NCATS NIH HHS
ID : UL1 TR001863
Pays : United States
Organisme : NIDDK NIH HHS
ID : U24 DK066116
Pays : United States
Organisme : NIDDK NIH HHS
ID : U24 DK082194
Pays : United States

Commentaires et corrections

Type : CommentIn

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Auteurs

Daryl J McLeod (DJ)

Section of Urology, Nationwide Children's Hospital, Columbus, OH, 43205, USA. Daryl.mcleod@nationwidechildrens.org.
Center for Surgical Outcomes Research, Nationwide Children's Hospital, Columbus, OH, 43205, USA. Daryl.mcleod@nationwidechildrens.org.

Yuri V Sebastião (YV)

Center for Surgical Outcomes Research, Nationwide Children's Hospital, Columbus, OH, 43205, USA.

Christina B Ching (CB)

Section of Urology, Nationwide Children's Hospital, Columbus, OH, 43205, USA.
Center for Clinical and Translational Research, Nationwide Children's Hospital, Columbus, OH, 43205, USA.

Jason H Greenberg (JH)

Department of Pediatrics, Section of Nephrology, Yale University School of Medicine, New Haven, CT, 06510, USA.

Susan L Furth (SL)

Department of Pediatrics, Division of Nephrology, Perelman School of Medicine at the University of Pennsylvania and the Children's Hospital of Philadelphia, Philadelphia, PA, 19104, USA.

Brian Becknell (B)

Center for Clinical and Translational Research, Nationwide Children's Hospital, Columbus, OH, 43205, USA.
Department of Pediatrics, Section of Nephrology, Nationwide Children's Hospital, Columbus, OH, 43205, USA.

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