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Kidney Week

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

Authors

  • 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
Background

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.

Methods

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).

Results

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).

Conclusion

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.