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Abstract: SA-PO980

Urine Ammonium Excretion Helps Identify High Dietary Acid Intake in Patients With Early-Stage CKD and Eubicarbonatemic Acidosis

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 and White Central Texas, Temple, Texas, United States
  • Madias, Nicolaos E., Tufts University School of Medicine, Boston, Massachusetts, United States
  • Mamun, Abdullah A., Baylor Scott & White Health, Dallas, Texas, United States
  • Simoni, Jan, Texas Tech University, Lubbock, Texas, United States
  • Wesson, Donald E., The University of Texas at Austin Dell Medical School, Austin, Texas, United States
Background

Better estimated glomerular filtration rate (eGFR) preservation in patients with Stage 2 chronic kidney disease (CKD) and normal plasma total CO2 (PTCO2) despite acid (H+) retention (i.e., with eubicarbonatemic acidosis) was associated with lower H+ retention. Reduced dietary H+ with ether oral NaHCO3 or base-producing foods reduced H+ retention and so dietary H+ reduction might be kidney-protective in this setting. Even so, tabulating food intake then estimating potential renal acid load (PRAL) is challenging in clinical settings. We explored if urine excretion of citrate (UcitV), a metabolite that defends against H+ accumulation, or ammonium (UNH4+V), a buffer whose urine excretion increases with an H+ challenge, can evaluate dietary H+ assessed by PRAL in patients with early-stage CKD (stage 2) and eubicarbonatemic acidosis for whom kidney protective interventions are most beneficial.

Methods

We measured 8-hour UcitV (8h UcitV) and 8-hour (8h UNH4+V) in 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 compared these urine parameters across groups and performed linear regressions (LR) with PRAL within groups. 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.

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 had lower 8h UcitV [1.00 (0.22) vs. 1.14 (0.03 mmol, p<0.01) but 8h UNH4+V (mEq/8h) was not different [14.1 (2.6) vs.14.7 (2.5), p=0.24)]. LR for 8h UcitV vs. PRAL was negative for CKD 1 (p<0.01, r2=0.15) and negative but not significant for CKD 2 (p=0.65, r2=0.01). LR for 8h UNH4+V was positive and significant for both CKD 1 (p<0.01, r2=0.14) and CKD 2 (p<0.01, r2=0.08). Adding UNH4+V to UcitV in the regression increased r2 for CKD 1 (0.15 to 0.21) but not CKD 2 (0.08 to 0.06).

Conclusion

In patients with CKD and eubicarbonatemic acidosis, UNH4+V was positively associated with dietary H+ intake as assessed by PRAL and should be further explored as an indicator of high dietary H+.