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 Twitter

Kidney Week

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


  • 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

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.


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.


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).


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.