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Abstract: SA-PO911

Effect of Sodium Bicarbonate on Acid Excretion and BP in Patients with and Without CKD: The Acid-Base Compensation in CKD (ABC) Study

Session Information

Category: CKD (Non-Dialysis)

  • 2102 CKD (Non-Dialysis): Clinical, Outcomes, and Trials

Authors

  • Tyson, Crystal C., Duke University Medical Center, Durham, North Carolina, United States
  • Lin, Pao-Hwa, Duke University Medical Center, Durham, North Carolina, United States
  • Luciano, Alison, Duke University, Durham, North Carolina, United States
  • Allen, Jenifer M., Duke University Medical Center, Durham, North Carolina, United States
  • Bowman, Cassandra, Duke University Medical Center, Durham, North Carolina, United States
  • Gung, Joseph, Duke University Medical Center, Durham, North Carolina, United States
  • Asplin, John R., Litholink Corp, Chicago, Illinois, United States
  • Pendergast, Jane F., Duke University, Durham, North Carolina, United States
  • Svetkey, Laura P., Duke University Medical Center, Durham, North Carolina, United States
  • Scialla, Julia J., Duke University Medical Center, Durham, North Carolina, United States
Background

As kidney function worsens, net acid excretion (NAE) diminishes resulting in subclinical, then overt, metabolic acidosis (MA). Treatment with alkali may improve outcomes in CKD even when overt MA is not present. Our goal was threefold: 1) evaluate NAE and response to alkali in the setting of controlled diet acid load; 2) compare response in those with and without CKD; and 3) evaluate change in 24h BP as a potential mechanism of benefit.

Methods

We enrolled 14 non-diabetic adults in a random order, cross-over feeding study; 8 had CKD and 6 did not. After a 3-day run-in, participants consumed a 7-day controlled acid load diet supplemented with NaHCO3 tablets (alkali; 31 or 39 mEq/day based on weight) and an identical 7-day diet supplemented with NaCl as table salt (control), in random order. We assessed NAE and other acidification markers from two 24h urines, and measured 24h ambulatory BP at the end of each period. We estimated the alkali effect using mixed models adjusted for CKD status, study period, and intervention order, and tested for interaction between alkali and CKD.

Results

Mean age was 68, 64% were women, and 57% were white. In the control period, mean NAE and urine citrate were lower for those with CKD (29.6±7.7 mEq/d and 388.4±213.5 mg/d) vs. non-CKD (40.4±18.6 mEq/d and 687.5±218.6 mg/d) on identical diets. Overall, alkali lowered NAE and urine ammonium and increased urine pH, HCO3 and citrate. Response in urine pH and citrate to alkali differed by CKD status. Alkali increased urine pH more in patients with vs. without CKD (p-int=0.17), whereas urine citrate increased only among those with CKD (p-int=0.05). Alkali had no effect on 24h BP (Table).

Conclusion

Despite identical diets, NAE and urine citrate are lower in CKD vs. non-CKD suggesting that NAE in CKD has non-diet determinants. NaHCO3 decreases NAE; however, it increases, thereby restoring, lower urine citrate in CKD. Urine citrate may be a useful marker of early, subclinical acidosis in CKD that responds to therapy.

Funding

  • NIDDK Support