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Tytuł:
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Urine citrate excretion as a marker of acid retention in patients with chronic kidney disease without overt metabolic acidosis.
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Autorzy:
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Goraya N; Baylor Scott & White Health Department of Internal Medicine, Temple, Texas, USA; Texas A&M Health Sciences Center College of Medicine, Temple, Texas, USA.
Simoni J; Texas Tech University Health Sciences Center Department of Surgery, Lubbock, Texas, USA.
Sager LN; Baylor Scott & White Health Department of Biostatistics, Temple, Texas, USA.
Madias NE; St. Elizabeth's Medical Center and Tufts University School of Medicine Department of Medicine, Boston, Massachusetts, USA.
Wesson DE; Baylor Scott & White Health Department of Internal Medicine, Dallas, Texas, USA; Texas A&M Health Sciences Center College of Medicine, Dallas, Texas, USA. Electronic address: .
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Źródło:
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Kidney international [Kidney Int] 2019 May; Vol. 95 (5), pp. 1190-1196. Date of Electronic Publication: 2019 Mar 01.
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Typ publikacji:
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Journal Article; Research Support, Non-U.S. Gov't
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Język:
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English
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Imprint Name(s):
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Publication: 2016- : New York : Elsevier
Original Publication: New York, Springer-Verlag.
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MeSH Terms:
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Acidosis/*diagnosis
Citric Acid/*urine
Kidney/*physiopathology
Renal Elimination/*physiology
Renal Insufficiency, Chronic/*complications
Acid-Base Equilibrium/physiology ; Acidosis/etiology ; Acidosis/urine ; Adult ; Biomarkers/urine ; Citric Acid/metabolism ; Disease Progression ; Feasibility Studies ; Female ; Glomerular Filtration Rate/physiology ; Humans ; Male ; Middle Aged ; Renal Insufficiency, Chronic/physiopathology ; Renal Insufficiency, Chronic/urine
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Contributed Indexing:
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Keywords: GFR; acidosis; bicarbonate; chronic kidney disease; diet
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Substance Nomenclature:
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0 (Biomarkers)
2968PHW8QP (Citric Acid)
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Entry Date(s):
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Date Created: 20190309 Date Completed: 20200402 Latest Revision: 20200402
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Update Code:
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20240105
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DOI:
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10.1016/j.kint.2018.11.033
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PMID:
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30846270
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Acid (H + ) retention appears to contribute to progressive decline in glomerular filtration rate (GFR) in patients with chronic kidney disease (CKD), including some patients without metabolic acidosis. Identification of patients with H + retention but without metabolic acidosis could facilitate targeted alkali therapy; however, current methods to assess H + retention are invasive and have little clinical utility. We tested the hypothesis that urine excretion of the pH-sensitive metabolite citrate can identify H + retention in patients with reduced GFR but without overt metabolic acidosis. H + retention was assessed based on the difference between observed and expected plasma total CO 2 after an oral sodium bicarbonate load. The association between H + retention and urine citrate excretion was evaluated in albuminuric CKD patients with eGFR 60-89 ml/min/1.73m 2 (CKD 2, n=40) or >90 ml/min/1.73m 2 (CKD 1, n = 26) before and after 30 days of base-producing fruits and vegetables. Baseline H + retention was higher in CKD 2, while baseline urine citrate excretion was lower in CKD 2 compared to CKD 1. Base-producing fruits and vegetables decreased H + retention in CKD 2 and increased urine citrate excretion in both groups. Thus, H + retention is associated with lower urine citrate excretion, and reduction of H + retention with a base-producing diet is associated with increased urine citrate excretion. These results support further exploration of the utility of urine citrate excretion to identify H + retention in CKD patients with reduced eGFR but without metabolic acidosis, to determine their candidacy for kidney protection with dietary H + reduction or alkali therapy.
(Copyright © 2019 International Society of Nephrology. Published by Elsevier Inc. All rights reserved.)
Comment in: Kidney Int. 2019 May;95(5):1020-1022. (PMID: 31010475)
