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Abstract: FR-OR41

Effect of Dietary Acid Reduction on Acid-Base Status of Patients with CKD but with Normal eGFR: A 5-Year Randomized Trial

Session Information

Category: CKD (Non-Dialysis)

  • 2302 CKD (Non-Dialysis): Clinical, Outcomes, and Trials

Authors

  • Goraya, Nimrit, Baylor Scott and White Central Texas, Temple, Texas, United States
  • Simoni, Jan, Texas Tech University System, Lubbock, Texas, United States
  • Kahlon, Maninder, The University of Texas at Austin Dell Medical School, Austin, Texas, United States
  • Aksan, Nazan, The University of Texas at Austin Dell Medical School, Austin, Texas, United States
  • Wesson, Donald E., The University of Texas at Austin Dell Medical School, Austin, Texas, United States
Background

Previous studies show that high acid-producing diets contribute to metabolic acidosis in subjects with chronic kidney disease (CKD) stage G3 and to eubicarbonatemic acidosis in those with stage G2, conditions of acid accumulation that have been associated with adverse outcomes. We tested the hypothesis that high acid-producing diets have discernible effects on acid-base status of those with CKD but with normal baseline eGFR.

Methods

One hundred fifty-three macroalbuminuric, non-diabetic G1 participants with eGFR (>90 ml/min/1.73 m2) and baseline high acid-producing diets (potential renal acid load [PRAL, mean (SE)] = 61.7 (0.83) mmol/day) were randomized to Usual Care (UC, n=51) or to base-producing fruits and vegetables (F+V, n=51) in amounts to reduce dietary PRAL by half, or oral NaHCO3 (HCO3, n=51) 0.4 mmol/kg bw/day. They were followed for 5 years, measuring eGFR (CKD-EPI equation) and plasma total CO2 (PTCO2) annually and the following at baseline and 5 years: plasma citrate (Pcit), 8-hour urine citrate excretion (UcitV), and acid retention by comparing observed to expected increase in PTCO2 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 values were similar among groups. For both F+V and HCO3 relative to UC, 5-year eGFR was higher ([mean (SE)], F+V [96.5(0.79)], HCO3 [95.9 (0.96)] vs. UC [92.1 (1.23), ml/min/1.73 m2, ps<0.001]). For both F+V and HCO3 relative to UC, 5-year PTCO2 was higher (PTCO2, F+V [26.7(0.08)], HCO3 [26.7 (0.08)] vs. UC [26.2 (0.09), mM, p<0.001]). For both F+V and HCO3 relative to UC, 5-year Pcit and UcitV, were higher (Pcit, F+V [0.159 (0.001)], HCO3 [0.158 (0.002)] vs. UC [0.157 (0.001), mmol/ml, p<0.02]; UcitV, F+V [1.163 (0.011)], HCO3 [1.141 (0.002)] vs. UC [1.124 (0.006), mmoles/8 hours, ps<0.05]). For both F+V and HCO3 relative to UC, 5-year acid retention was lower (acid retention, F+V [-1.19(1.61)], HCO3 [-1.72 (1.58)] vs. UC [5.23 (1.55), mmol, ps<0.003]).

Conclusion

In participants with CKD and normal eGFR eating high acid-producing diets at baseline, dietary acid reduction over 5 years with either F+V or NaHCO3 yielded small but discernible improvements in acid-base status that might mediate slower CKD progression.