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Kidney Int. 2019 May;95(5):1190-1196. doi: 10.1016/j.kint.2018.11.033. Epub 2019 Mar 1.

Urine citrate excretion as a marker of acid retention in patients with chronic kidney disease without overt metabolic acidosis.

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Baylor Scott & White Health Department of Internal Medicine, Temple, Texas, USA; Texas A&M Health Sciences Center College of Medicine, Temple, Texas, USA.
Texas Tech University Health Sciences Center Department of Surgery, Lubbock, Texas, USA.
Baylor Scott & White Health Department of Biostatistics, Temple, Texas, USA.
St. Elizabeth's Medical Center and Tufts University School of Medicine Department of Medicine, Boston, Massachusetts, USA.
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:


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 CO2 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/1.73m2 (CKD 2, n=40) or >90 ml/min/1.73m2 (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.


GFR; acidosis; bicarbonate; chronic kidney disease; diet


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