ASN's Mission

To create a world without kidney diseases, the ASN Alliance for Kidney Health elevates care by educating and informing, driving breakthroughs and innovation, and advocating for policies that create transformative changes in kidney medicine throughout the world.

learn more

Contact ASN

1401 H St, NW, Ste 900, Washington, DC 20005


The Latest on X

Kidney Week

Please note that you are viewing an archived section from 2022 and some content may be unavailable. To unlock all content for 2022, please visit the archives.

Abstract: SA-PO982

Urine Citrate Excretion Better Identifies Eubicarbonatemic Acidosis Than Plasma Acid-Base Parameters in Patients With CKD

Session Information

  • CKD: Pathobiology - II
    November 05, 2022 | Location: Exhibit Hall, Orange County Convention Center‚ West Building
    Abstract Time: 10:00 AM - 12:00 PM

Category: CKD (Non-Dialysis)

  • 2203 CKD (Non-Dialysis): Mechanisms


  • Goraya, Nimrit, Baylor Scott & White Medical Center Temple, Temple, Texas, United States
  • Madias, Nicolaos E., Tufts Medical Center, Boston, Massachusetts, United States
  • Mamun, Abdullah A., Baylor Scott & White Health, Dallas, Texas, United States
  • Wesson, Donald E., Dell Seton Medical Center at The University of Texas, Austin, Texas, United States
  • Simoni, Jan, Texas Tech University Health Sciences Center, Lubbock, Texas, United States

Acid (H+) mitigating mechanisms help maintain normal plasma total CO2 (PTCO2) in patients with chronic kidney disease (CKD) and reduced estimated glomerular filtration rate (eGFR) despite H+ retention or positive H+ balance (i.e., eubicarbonatemic acidosis). Current guidelines recommend oral alkali treatment of metabolic acidosis in CKD only for patients with PTCO2 < 22 mM, thereby excluding those with eubicarbonatemic acidosis for whom oral alkali might slow CKD progression (AJP 317: F502, 2019). We tested if variances in urine excretion of citrate (UcitV), a metabolite that defends against H+ retention, better identifies eubicarbonatemic acidosis in early-stage CKD (stage 2) than variances in plasma acid-base parameters.


We compared H+ retention, plasma acid-base parameters, and UcitV between participants with PTCO2 ≥22 mM and CKD 2 (eGFR [mean (SD) ml/min/1.73 m2] =73.8 (6.3), n=167) or CKD 1 [eGFR=99.2 (7.3), n=62] due to macroalbuminuric, non-diabetic nephropathy. We assessed H+ retention by comparing observed to expected increase in PTCO2 in response to retained HCO3- (dose-urine excretion) 2 hours after an oral NaHCO3 bolus (0.5 mEq/Kg bw), assuming 50% body weight HCO3- space of distribution. We measured venous plasma bicarbonate (PHCO3-), PCO2, pH (PpH), PTCO2 , and 8-hour UcitV (8h UcitV).


H+ retention [mean (SD), mmol)] was higher in CKD 2 than CKD 1 [18.2 (12.4) vs. 3.8 (12.5), mmol, p<0.01]. CKD 2 vs. CKD 1 participants had lower PTCO2 [25.2 (1.2) vs. 25.9 (1.2) mM, p<0.01], PHCO3- [24.0 (1.3) vs. 24.7 (1.2) mE/l, p<0.01], PCO2 [40.1 (1.2) vs. 41.0 (0.9) mm Hg, p<0.01] but no difference in PpH [7.397 (0.014) vs. 7.399 (0.016), p=0.31]. CKD 2 vs. CKD 1 8h UcitV was lower [1.00 (0.22) vs. 1.14 (0.03) mmol, p<0.01).


Substantially greater H+ retention in CKD 2 than CKD 1 participants was associated with statistically but quantitatively minor decreases in plasma acid-base parameters, supporting the effectiveness of body mechanisms that mitigate against retained H+ but challenging utility of plasma acid-base parameters to identify eubicarbonatemic acidosis. Conversely, UcitV was both statistically and substantially lower in CKD 2 than CKD 1, supporting this parameter as a better indicator of eubicarbonatemic acidosis in patients with early-stage CKD.