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Abstract: FR-PO201

Urine Citrate Excretion Non-Invasively Identifies Changes in Acid Retention over Time in CKD 2 Patients Without Metabolic Acidosis

Session Information

Category: CKD (Non-Dialysis)

  • 1901 CKD (Non-Dialysis): Epidemiology, Risk Factors, and Prevention

Authors

  • Goraya, Nimrit, Baylor Scott and White Health, Temple, Texas, United States
  • Simoni, Jan, Texas Tech University Health Sciences Center, Lubbock, Texas, United States
  • Sager, Lauren N., Baylor Scott & White, Temple, Texas, United States
  • Madias, Nicolaos E., Tufts University School of Medicine, Boston, Massachusetts, United States
  • Wesson, Donald E., Baylor Scott and White Health and Wellness Center, Dallas, Texas, United States
Background

Some CKD stage 2 (eGFR=60-89 ml/min/1.73 m2, CKD 2) patients without metabolic acidosis (conventionally defined as plasma total CO2 <22 mM) nevertheless have acid (H+) retention that appears to exacerbate nephropathy progression, increases as eGFR decreases over time (Goraya et al, AJP, 2018), and this increase in H+ retention might be ameliorated with chronic oral NaHCO3. Current methods to measure H+ retention are cumbersome and invasive so we explored the utility of urine citrate excretion to non-invasively identify changes in H+ retention over time.

Methods

We measured H+ retention and 8-hour urine citrate excretion (UcitrateV) in macroalbuminuric, non-diabetic CKD 2 patients with hypertension-associated nephropathy without metabolic acidosis (plasma total CO2 >24 mM) given 0.5 meq/kg bw/day NaHCO3 (HCO3, n=40), 0.5 meq/kg bw/day NaCl (NaCl, n=40), or usual care (UC, n=40) and assessed them yearly for 10 years. H+ retention was measured at baseline and 10 years by comparing observed to expected increase in plasma total CO2 in response to retained HCO3 (dose minus UHCO3V) 2 hours after oral NaHCO3 bolus (0.5 mmol/kg bw), assuming 50% body weight HCO3 apparent space of distribution.

Results

Baseline H+ retention and UcitrateV were not different among groups. The 10-year vs. respective baseline value in HCO3 was not different for H+ retention (15.7±12.6 vs. 18.1±14.9 mmol, p=0.90) or UcitrateV (204±43 vs. 195±49 mg, respectively, p=0.30). By contrast, the 10-year vs. respective baseline value in NaCl was higher for H+ retention (27.5±15.2 vs. 19.2±16.7 mmol, respectively, p<0.01) and lower for UcitrateV (158±47 vs. 193±52 mg, respectively, p<0.01). Similar to NaCl, 10-year vs. respective baseline value in UC was higher for H+ retention (22.1±11.2 vs. 17.4±9.9 mmol, respectively, p<0.01) and lower for UcitrateV (164±42 vs. 187±40 mg, respectively, p<0.01). A generalized linear model for repeated measures, adjusted for time, showed that UcitrateV was a predictor of H+ retention overall (p<0.01) and within each of the 3 groups (p<0.05).

Conclusion

UcitrateV non-invasively identifies changes in H+ retention over time in CKD 2 patients without metabolic acidosis. It should be further explored to follow clinical effectiveness of dietary H+ reduction in CKD patients without metabolic acidosis.