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Kidney Week

Abstract: FR-PO200

Urine Citrate Excretion Non-Invasively Verifies Reduced Acid Retention in Response to Dietary Acid Reduction 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 (defined as plasma total CO2 <22 mM) nevertheless have acid (H+) retention and decreasing H+ retention with dietary H+ reduction slows eGFR decline. Current methods to verify a decrease in H+ retention and thereby establish clinical effectiveness of dietary H+ reduction require cumbersome and invasive methods with limited clinical utility. We explored the utility of urine citrate excretion to non-invasively verify decreased H+ retention in response to dietary H+ reduction in CKD 2 patients without metabolic acidosis.


We measured H+ retention and 8-hour urine citrate excretion (UcitrateV) in macroalbuminuric, non-diabetic CKD 2 (n=40) and CKD stage 1 (eGFR >90 ml/min/1.73 m2, CKD 1, n=26) patients with hypertension-associated nephropathy but without metabolic acidosis (mean plasma total CO2 25.9±0.8 and 26.4±0.6 mM, respectively). H+ retention was measured before and after dietary H+ reduction with 30 days of base-producing fruits and vegetables (F+V) by comparing observed to expected increase in plasma [HCO3] in response to retained HCO3 (dose minus UHCO3V) 6 hours after oral NaHCO3 bolus (0.5 mmol/kg bw), assuming 50% body weight HCO3 apparent space of distribution.


H+ retention was higher in CKD 2 than CKD 1 (28.1±9.4 vs. 5.2±12.0 mmol, respectively, p<0.01) but UcitrateV was lower in CKD 2 than CKD 1 (187±40 vs. 335±125 mg, respectively, p<0.01). F+V did not decrease H+ retention in CKD 1 (p=0.88) but did so in CKD 2 (to 18.4±17.4 mmol, p<0.01 vs. baseline) and increased UcitrateV (to 245±70 mg, p<0.01 vs. baseline) in CKD 2. Overall Pearson Correlation for UcitrateV with H+ retention after F+V was -0.71 (p<0.001). A mixed effects regression model showed UcitrateV to be strongly predictive of H+ retention (p<0.001) so that for every 1 mg increase in UcitrateV, H+ retention decreased 0.096 mmol.


UcitrateV non-invasively verifies decreased H+ retention in response to 30 days of F+V in CKD 2 patients without metabolic acidosis. It should be further explored as a method to establish clinical effectiveness of dietary H+ reduction in CKD patients with comparatively well-preserved eGFR and no metabolic acidosis, but who are at risk for nephropathy progression.