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

• CKD: Epidemiology, Risk Factors, Prevention - II
  October 26, 2018 | Location: Exhibit Hall, San Diego Convention Center
  Abstract Time: 10:00 AM - 12:00 PM

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

Nimrit Goraya,

• Simoni, Jan, Texas Tech University Health Sciences Center, Lubbock, Texas, United States

Jan Simoni,

• Sager, Lauren N., Baylor Scott & White, Temple, Texas, United States

Lauren N. Sager,

• Madias, Nicolaos E., Tufts University School of Medicine, Boston, Massachusetts, United States

Nicolaos E. Madias,

• Wesson, Donald E., Baylor Scott and White Health and Wellness Center, Dallas, Texas, United States

Donald E. Wesson,

Background

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.

Methods

We measured H⁺ retention and 8-hour urine citrate excretion (U_citrateV) 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 U_HCO3V) 6 hours after oral NaHCO₃ bolus (0.5 mmol/kg bw), assuming 50% body weight HCO₃ apparent space of distribution.

Results

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 U_citrateV 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 U_citrateV (to 245±70 mg, p<0.01 vs. baseline) in CKD 2. Overall Pearson Correlation for U_citrateV with H⁺ retention after F+V was -0.71 (p<0.001). A mixed effects regression model showed U_citrateV to be strongly predictive of H⁺ retention (p<0.001) so that for every 1 mg increase in U_citrateV, H⁺ retention decreased 0.096 mmol.

Conclusion

U_citrateV 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.