Low Serum Bicarbonate and CKD Progression in Children.

acidosis alkalis anemia bicarbonates chronic chronic kidney disease chronic metabolic acidosis demography glomerular filtration rate hypertension longitudinal studies pediatrics phosphates proteinuria renal insufficiency renal progression renal replacement therapy

Journal

Clinical journal of the American Society of Nephrology : CJASN
ISSN: 1555-905X
Titre abrégé: Clin J Am Soc Nephrol
Pays: United States
ID NLM: 101271570

Informations de publication

Date de publication:
08 06 2020
Historique:
received: 14 06 2019
accepted: 09 04 2020
pubmed: 30 5 2020
medline: 21 10 2021
entrez: 30 5 2020
Statut: ppublish

Résumé

Studies of adults have demonstrated an association between metabolic acidosis, as measured by low serum bicarbonate levels, and CKD progression. We evaluated this relationship in children using data from the Chronic Kidney Disease in Children study. The relationship between serum bicarbonate and a composite end point, defined as 50% decline in eGFR or KRT, was described using parametric and semiparametric survival methods. Analyses were stratified by underlying nonglomerular and glomerular diagnoses, and adjusted for demographic characteristics, eGFR, proteinuria, anemia, phosphate, hypertension, and alkali therapy. Six hundred and three participants with nonglomerular disease contributed 2673 person-years of follow-up, and 255 with a glomerular diagnosis contributed 808 person-years of follow-up. At baseline, 39% (237 of 603) of participants with nonglomerular disease had a bicarbonate level of ≤22 meq/L and 36% (85 of 237) of those participants reported alkali therapy treatment. In participants with glomerular disease, 31% (79 of 255) had a bicarbonate of ≤22 meq/L, 18% (14 of 79) of those participants reported alkali therapy treatment. In adjusted longitudinal analyses, compared with participants with a bicarbonate level >22 meq/L, hazard ratios associated with a bicarbonate level of <18 meq/L and 19-22 meq/L were 1.28 [95% confidence interval (95% CI), 0.84 to 1.94] and 0.91 (95% CI, 0.65 to 1.26), respectively, in children with nonglomerular disease. In children with glomerular disease, adjusted hazard ratios associated with bicarbonate level ≤18 meq/L and bicarbonate 19-22 meq/L were 2.16 (95% CI, 1.05 to 4.44) and 1.74 (95% CI, 1.07 to 2.85), respectively. Resolution of low bicarbonate was associated with a lower risk of CKD progression compared with persistently low bicarbonate (≤22 meq/L). In children with glomerular disease, low bicarbonate was linked to a higher risk of CKD progression. Resolution of low bicarbonate was associated with a lower risk of CKD progression. Fewer than one half of all children with low bicarbonate reported treatment with alkali therapy. Long-term studies of alkali therapy's effect in patients with pediatric CKD are needed.

Sections du résumé

BACKGROUND AND OBJECTIVES
Studies of adults have demonstrated an association between metabolic acidosis, as measured by low serum bicarbonate levels, and CKD progression. We evaluated this relationship in children using data from the Chronic Kidney Disease in Children study.
DESIGN, SETTING, PARTICIPANTS, & MEASUREMENTS
The relationship between serum bicarbonate and a composite end point, defined as 50% decline in eGFR or KRT, was described using parametric and semiparametric survival methods. Analyses were stratified by underlying nonglomerular and glomerular diagnoses, and adjusted for demographic characteristics, eGFR, proteinuria, anemia, phosphate, hypertension, and alkali therapy.
RESULTS
Six hundred and three participants with nonglomerular disease contributed 2673 person-years of follow-up, and 255 with a glomerular diagnosis contributed 808 person-years of follow-up. At baseline, 39% (237 of 603) of participants with nonglomerular disease had a bicarbonate level of ≤22 meq/L and 36% (85 of 237) of those participants reported alkali therapy treatment. In participants with glomerular disease, 31% (79 of 255) had a bicarbonate of ≤22 meq/L, 18% (14 of 79) of those participants reported alkali therapy treatment. In adjusted longitudinal analyses, compared with participants with a bicarbonate level >22 meq/L, hazard ratios associated with a bicarbonate level of <18 meq/L and 19-22 meq/L were 1.28 [95% confidence interval (95% CI), 0.84 to 1.94] and 0.91 (95% CI, 0.65 to 1.26), respectively, in children with nonglomerular disease. In children with glomerular disease, adjusted hazard ratios associated with bicarbonate level ≤18 meq/L and bicarbonate 19-22 meq/L were 2.16 (95% CI, 1.05 to 4.44) and 1.74 (95% CI, 1.07 to 2.85), respectively. Resolution of low bicarbonate was associated with a lower risk of CKD progression compared with persistently low bicarbonate (≤22 meq/L).
CONCLUSIONS
In children with glomerular disease, low bicarbonate was linked to a higher risk of CKD progression. Resolution of low bicarbonate was associated with a lower risk of CKD progression. Fewer than one half of all children with low bicarbonate reported treatment with alkali therapy. Long-term studies of alkali therapy's effect in patients with pediatric CKD are needed.

Identifiants

pubmed: 32467307
pii: 01277230-202006000-00006
doi: 10.2215/CJN.07060619
pmc: PMC7274283
doi:

Substances chimiques

Bicarbonates 0
Buffers 0

Types de publication

Journal Article Research Support, N.I.H., Extramural Research Support, Non-U.S. Gov't

Langues

eng

Sous-ensembles de citation

IM

Pagination

755-765

Subventions

Organisme : NIDDK NIH HHS
ID : R01 DK118015
Pays : United States
Organisme : NIDDK NIH HHS
ID : U01 DK066143
Pays : United States
Organisme : NIDDK NIH HHS
ID : R03 DK105242
Pays : United States
Organisme : NIDDK NIH HHS
ID : U01 DK066174
Pays : United States
Organisme : NICHD NIH HHS
ID : R01 HD091185
Pays : United States
Organisme : NIDDK NIH HHS
ID : U24 DK082194
Pays : United States
Organisme : NIDDK NIH HHS
ID : U24 DK066116
Pays : United States
Organisme : NIDDK NIH HHS
ID : T32 DK007110
Pays : United States

Informations de copyright

Copyright © 2020 by the American Society of Nephrology.

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Auteurs

Denver D Brown (DD)

Division of Pediatric Nephrology, Children's National Hospital, Washington, DC.

Jennifer Roem (J)

Johns Hopkins Bloomberg School of Public Health, Baltimore, Maryland.

Derek K Ng (DK)

Johns Hopkins Bloomberg School of Public Health, Baltimore, Maryland.

Kimberly J Reidy (KJ)

Division of Pediatric Nephrology, The Children's Hospital at Montefiore, Bronx, New York.

Juhi Kumar (J)

Division of Pediatric Nephrology, Weill Cornell Medicine, New York, New York.

Matthew K Abramowitz (MK)

Department of Medicine, Albert Einstein College of Medicine, Bronx, New York.

Robert H Mak (RH)

Division of Pediatric Nephrology, Rady Children's Hospital San Diego, University of California San Diego, San Diego, California.

Susan L Furth (SL)

Division of Pediatric Nephrology, The Children's Hospital of Philadelphia, Philadelphia, Pennsylvania.

George J Schwartz (GJ)

Division of Pediatric Nephrology, University of Rochester, Rochester, New York.

Bradley A Warady (BA)

Division of Pediatric Nephrology, Children's Mercy Hospital, Kansas City, Missouri.

Frederick J Kaskel (FJ)

Division of Pediatric Nephrology, The Children's Hospital at Montefiore, Bronx, New York.

Michal L Melamed (ML)

Department of Medicine, Albert Einstein College of Medicine, Bronx, New York.

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