Urinary DKK3 as a biomarker for short-term kidney function decline in children with chronic kidney disease: an observational cohort study.


Journal

The Lancet. Child & adolescent health
ISSN: 2352-4650
Titre abrégé: Lancet Child Adolesc Health
Pays: England
ID NLM: 101712925

Informations de publication

Date de publication:
06 2023
Historique:
received: 10 11 2022
revised: 04 02 2023
accepted: 09 02 2023
medline: 22 5 2023
pubmed: 30 4 2023
entrez: 29 4 2023
Statut: ppublish

Résumé

Childhood-onset chronic kidney disease is a progressive condition that can have a major effect on life expectancy and quality. We evaluated the usefulness of the kidney tubular cell stress marker urinary Dickkopf-related protein 3 (DKK3) in determining the short-term risk of chronic kidney disease progression in children and identifying those who will benefit from specific nephroprotective interventions. In this observational cohort study, we assessed the association between urinary DKK3 and the combined kidney endpoint (ie, the composite of 50% reduction of the estimated glomerular filtration rate [eGFR] or progression to end-stage kidney disease) or the risk of kidney replacement therapy (ie, dialysis or transplantation), and the interaction of the combined kidney endpoint with intensified blood pressure reduction in the randomised controlled ESCAPE trial. Moreover, urinary DKK3 and eGFR were quantified in children aged 3-18 years with chronic kidney disease and urine samples available enrolled in the prospective multicentre ESCAPE (NCT00221845; derivation cohort) and 4C (NCT01046448; validation cohort) studies at baseline and at 6-monthly follow-up visits. Analyses were adjusted for age, sex, hypertension, systolic blood pressure SD score (SDS), BMI SDS, albuminuria, and eGFR. 659 children were included in the analysis (231 from ESCAPE and 428 from 4C), with 1173 half-year blocks in ESCAPE and 2762 in 4C. In both cohorts, urinary DKK3 above the median (ie, >1689 pg/mg creatinine) was associated with significantly greater 6-month eGFR decline than with urinary DKK3 at or below the median (-5·6% [95% CI -8·6 to -2·7] vs 1·0% [-1·9 to 3·9], p<0·0001, in ESCAPE; -6·2% [-7·3 to -5·0] vs -1·5% [-2·9 to -0·1], p<0·0001, in 4C), independently of diagnosis, eGFR, and albuminuria. In ESCAPE, the beneficial effect of intensified blood pressure control was limited to children with urinary DKK3 higher than 1689 pg/mg creatinine, in terms of the combined kidney endpoint (HR 0·27 [95% CI 0·14 to 0·55], p=0·0003, number needed to treat 4·0 [95% CI 3·7 to 4·4] vs 250·0 [66·9 to ∞]) and the need for kidney replacement therapy (HR 0·33 [0·13 to 0·85], p=0·021, number needed to treat 6·7 [6·1 to 7·2] vs 31·0 [27·4 to 35·9]). In 4C, inhibition of the renin-angiotensin-aldosterone system resulted in significantly lower urinary DKK3 concentrations (least-squares mean 12 235 pg/mg creatinine [95% CI 10 036 to 14 433] in patients not on angiotensin-converting enzyme inhibitors or angiotensin 2 receptor blockers vs 6861 pg/mg creatinine [5616 to 8106] in those taking angiotensin-converting enzyme inhibitors or angiotensin 2 receptor blockers, p<0·0001). Urinary DKK3 indicates short-term risk of declining kidney function in children with chronic kidney disease and might allow a personalised medicine approach by identifying those who benefit from pharmacological nephroprotection, such as intensified blood pressure lowering. None.

Sections du résumé

BACKGROUND
Childhood-onset chronic kidney disease is a progressive condition that can have a major effect on life expectancy and quality. We evaluated the usefulness of the kidney tubular cell stress marker urinary Dickkopf-related protein 3 (DKK3) in determining the short-term risk of chronic kidney disease progression in children and identifying those who will benefit from specific nephroprotective interventions.
METHODS
In this observational cohort study, we assessed the association between urinary DKK3 and the combined kidney endpoint (ie, the composite of 50% reduction of the estimated glomerular filtration rate [eGFR] or progression to end-stage kidney disease) or the risk of kidney replacement therapy (ie, dialysis or transplantation), and the interaction of the combined kidney endpoint with intensified blood pressure reduction in the randomised controlled ESCAPE trial. Moreover, urinary DKK3 and eGFR were quantified in children aged 3-18 years with chronic kidney disease and urine samples available enrolled in the prospective multicentre ESCAPE (NCT00221845; derivation cohort) and 4C (NCT01046448; validation cohort) studies at baseline and at 6-monthly follow-up visits. Analyses were adjusted for age, sex, hypertension, systolic blood pressure SD score (SDS), BMI SDS, albuminuria, and eGFR.
FINDINGS
659 children were included in the analysis (231 from ESCAPE and 428 from 4C), with 1173 half-year blocks in ESCAPE and 2762 in 4C. In both cohorts, urinary DKK3 above the median (ie, >1689 pg/mg creatinine) was associated with significantly greater 6-month eGFR decline than with urinary DKK3 at or below the median (-5·6% [95% CI -8·6 to -2·7] vs 1·0% [-1·9 to 3·9], p<0·0001, in ESCAPE; -6·2% [-7·3 to -5·0] vs -1·5% [-2·9 to -0·1], p<0·0001, in 4C), independently of diagnosis, eGFR, and albuminuria. In ESCAPE, the beneficial effect of intensified blood pressure control was limited to children with urinary DKK3 higher than 1689 pg/mg creatinine, in terms of the combined kidney endpoint (HR 0·27 [95% CI 0·14 to 0·55], p=0·0003, number needed to treat 4·0 [95% CI 3·7 to 4·4] vs 250·0 [66·9 to ∞]) and the need for kidney replacement therapy (HR 0·33 [0·13 to 0·85], p=0·021, number needed to treat 6·7 [6·1 to 7·2] vs 31·0 [27·4 to 35·9]). In 4C, inhibition of the renin-angiotensin-aldosterone system resulted in significantly lower urinary DKK3 concentrations (least-squares mean 12 235 pg/mg creatinine [95% CI 10 036 to 14 433] in patients not on angiotensin-converting enzyme inhibitors or angiotensin 2 receptor blockers vs 6861 pg/mg creatinine [5616 to 8106] in those taking angiotensin-converting enzyme inhibitors or angiotensin 2 receptor blockers, p<0·0001).
INTERPRETATION
Urinary DKK3 indicates short-term risk of declining kidney function in children with chronic kidney disease and might allow a personalised medicine approach by identifying those who benefit from pharmacological nephroprotection, such as intensified blood pressure lowering.
FUNDING
None.

Identifiants

pubmed: 37119829
pii: S2352-4642(23)00049-4
doi: 10.1016/S2352-4642(23)00049-4
pii:
doi:

Substances chimiques

Creatinine AYI8EX34EU
Angiotensin-Converting Enzyme Inhibitors 0
Biomarkers 0
Angiotensins 0
DKK3 protein, human 0
Adaptor Proteins, Signal Transducing 0

Banques de données

ClinicalTrials.gov
['NCT00221845']

Types de publication

Randomized Controlled Trial Observational Study Journal Article Research Support, Non-U.S. Gov't

Langues

eng

Sous-ensembles de citation

IM

Pagination

405-414

Commentaires et corrections

Type : CommentIn

Informations de copyright

Copyright © 2023 Elsevier Ltd. All rights reserved.

Déclaration de conflit d'intérêts

Declaration of interests DF is affiliated with DiaRen. All other authors declare no competing interests.

Auteurs

Thimoteus Speer (T)

Department of Internal Medicine 4, Nephrology, Goethe-University, Frankfurt, Germany; Else Kroener Fresenius Center for Nephrological Research, Goethe-University, Frankfurt, Germany.

Stefan J Schunk (SJ)

Department of Internal Medicine IV, Saarland University Medical Center, Homburg/Saar, Germany.

Tamim Sarakpi (T)

Department of Internal Medicine 4, Nephrology, Goethe-University, Frankfurt, Germany.

David Schmit (D)

Department of Internal Medicine IV, Saarland University Medical Center, Homburg/Saar, Germany.

Martina Wagner (M)

Department of Internal Medicine IV, Saarland University Medical Center, Homburg/Saar, Germany.

Ludger Arnold (L)

Department of Internal Medicine IV, Saarland University Medical Center, Homburg/Saar, Germany.

Stephen Zewinger (S)

Department of Internal Medicine IV, Saarland University Medical Center, Homburg/Saar, Germany.

Karolis Azukaitis (K)

Clinic of Pediatrics, Institute of Clinical Medicine, Faculty of Medicine, Vilnius University, Vilnius, Lithuania.

Aysun Bayazit (A)

Department of Pediatric Nephrology, Cukurova University, Adana, Turkey.

Lukasz Obrycki (L)

Department of Nephrology, Kidney Transplantation and Hypertension, The Children's Memorial Health Institute, Warsaw, Poland.

Ipek Kaplan Bulut (I)

Department of Pediatrics, Faculty of Medicine, Ege University, Izmir, Turkey.

Ali Duzova (A)

Division of Pediatric Nephrology, Hacettepe University Faculty of Medicine, Ankara, Turkey.

Anke Doyon (A)

Division of Pediatric Nephrology, Center for Pediatrics and Adolescent Medicine, Heidelberg University Hospital, Heidelberg, Germany.

Bruno Ranchin (B)

Pediatric Nephrology Unit, Hôpital Femme Mère Enfant, Hospices Civils de Lyon, Université de Lyon, Lyon, France.

Salim Caliskan (S)

Department of Pediatric Nephrology, Cerrahpasa Faculty of Medicine, Istanbul University-Cerrahpasa, Istanbul, Turkey.

Jerome Harambat (J)

Pediatrics Department, Centre Hospitalier Universitaire de Bordeaux, Bordeaux, France.

Alev Yilmaz (A)

Pediatric Nephrology, Istanbul Medical Faculty, Istanbul, Turkey.

Harika Alpay (H)

Department of Pediatrics, School of Medicine, Marmara University, Istanbul, Turkey.

Francesca Lugani (F)

Pediatric Nephrology, IRCCS Istituto Giannina Gaslini, Genova, Italy.

Ayse Balat (A)

Department of Pediatric Nephrology, Gaziantep University, Gaziantep, Turkey.

Klaus Arbeiter (K)

Department of Pediatrics and Adolescent Medicine, Medical University of Vienna, Vienna, Austria.

Germana Longo (G)

Pediatric Nephrology, Dialysis and Transplant Unit, Department of Woman and Child Health, Azienda Ospedaliera-University of Padova, Padova, Italy.

Anette Melk (A)

Department of Kidney, Liver and Metabolic Diseases, Hannover Medical School, Hannover, Germany.

Uwe Querfeld (U)

Department of Pediatrics, Division of Gastroenterology, Nephrology and Metabolic Medicine, Charité - Universitätsmedizin Berlin, corporate member of Freie Universität Berlin, and Humboldt-Universität zu Berlin, Berlin, Germany.

Elke Wühl (E)

Division of Pediatric Nephrology, Center for Pediatrics and Adolescent Medicine, Heidelberg University Hospital, Heidelberg, Germany.

Otto Mehls (O)

Division of Pediatric Nephrology, Center for Pediatrics and Adolescent Medicine, Heidelberg University Hospital, Heidelberg, Germany.

Danilo Fliser (D)

Department of Internal Medicine IV, Saarland University Medical Center, Homburg/Saar, Germany; DiaRen, Homburg/Saar, Germany.

Franz Schaefer (F)

Division of Pediatric Nephrology, Center for Pediatrics and Adolescent Medicine, Heidelberg University Hospital, Heidelberg, Germany. Electronic address: franz.schaefer@med.uni-heidelberg.de.

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Classifications MeSH