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 X

Kidney Week

Please note that you are viewing an archived section from 2023 and some content may be unavailable. To unlock all content for 2023, please visit the archives.

Abstract: TH-PO925

Dietary Acid Reduction with Either Fruits and Vegetables or Oral NaHCO3, Adjuvant to Angiotensin-Converting Enzyme Inhibition, Slows Progression of Macroalbuminuric Stage G1 CKD

Session Information

Category: Health Maintenance, Nutrition, and Metabolism

  • 1500 Health Maintenance, Nutrition, and Metabolism


  • 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, 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, Austin, Texas, United States

Patients with macroalbuminuric (urine albumin-to-creatinine ratio > 200 mg/g creatinine) chronic kidney disease (CKD) are at increased progression risk despite angiotensin converting enzyme inhibition (ACEI). As high acid-producing diets are associated with risk for CKD progression, we tested the hypothesis that dietary acid reduction with either base-producing fruits and vegetables (F+V) or oral NaHCO3 (HCO3) slows progression in macroalbuminuric CKD with initially normal eGFR (> 90 ml/min/m2 or stage G1).


One hundred fifty-three macroalbuminuric, non-diabetic G1 participants on ACEI were randomized to F+V (n=51) in amounts to reduce dietary potential renal acid load 50%, oral NaHCO3 (HCO3, n=51) 0.4 meq/Kg bw/day, or no additional intervention (Usual Care,n=51). They were followed annually for 5 years, measuring eGFR and these urine parameters per g creatinine: albumin (Ualb), N-acetyl-D-glucosaminidase (UNAG, indicator of tubulointerstitial injury), angiotensinogen (UAGT, index of kidney angiotensin II), and isoprostane 8-isoprostaglandin F2α (U8-iso, index of systemic oxidative stress). Mixed linear regressions with random person intercepts tested differential group trajectories, p-values from the relevant interaction terms are included below.


We highlight group differences at year-5 for brevity and provide p-values from the full model. For 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]). 5-year Ualb and UNAG were lower in F+V and HCO3 than UC (Ualb, F+V [306 (8.5)], HCO3 [308 (8.4)], UC [416 (15)], mg/g, ps<0.001); UNAG, F+V [2.5 (0.05)], HCO3 [2.5 (0.05)], UC [2.8 (0.06)], U/g, ps<0.001). Additionaly, 5-year UAGT and U8-iso were lower in F+V and HCO3 than UC (UATG, F+V [20.9 (0.32)], HCO3 [20.6 (0.35)], UC, [23.1 (0.40), µg/g, ps<0.001]; 8-iso, F+V [1.08 (0.02)], HCO3 [1.06 (0.02)] vs. UC [1.27 (0.03)], µg/g, ps<0.001]).


Dietary acid reduction with either F+V or NaHCO3, adjunctive to ACEI, yielded better eGFR preservation than UC in macroalbuminuric G1 CKD, associated with reductions of indicators of kidney angiotensin II and systemic oxidative stress, each potential mediators of CKD progression.