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Abstract: PO0386

Acid-Base Status More Than Dietary Acid Intake Determines Urine Citrate Excretion in CKD

Session Information

Category: Bone and Mineral Metabolism

  • 402 Bone and Mineral Metabolism: Clinical

Authors

  • Goraya, Nimrit, Baylor Scott and White Central Texas, Temple, Texas, United States
  • Madias, Nicolaos E., Tufts University School of Medicine, Boston, Massachusetts, United States
  • Mamun, Abdullah A., Baylor Scott and White Health and Wellness Center, Dallas, Texas, United States
  • Simoni, Jan, Surgery, Texas Tech University HSC, Lubbock, Texas, United States
  • Wesson, Donald E., Baylor Scott and White Health and Wellness Center, Dallas, Texas, United States
Background

Lower urine excretion of the pH-sensitive metabolite citrate (UcitV) might be a clinically useful biomarker of steady-state acid (H+) retention not evident by plasma acid-base parameters in patients with CKD. Ongoing dietary H+ intake might also be an important determinant of UcitV and possibly confound its utility as a biomarker of underlying H+ retention.

Methods

We examined the influence on 8-hour UcitV (UcitV), its plasma citrate concentration (Pcit) and kidney clearance (UcitV/Pcit) components, and 8-hour urine net acid excretion (8h NAE) of 1) ongoing dietary acid addition assessed by potential renal acid load (PRAL) and 2) steady-state acid-base status assessed by plasma total CO2 (PTCO2) and by H+ retention [estimated by comparing observed to expected PTCO2 increase in response to retained HCO3 (administered minus UHCO3V) 2 hours after oral NaHCO3 bolus (0.5 mmol/kg bw), assuming 50% body wt HCO3 apparent space of distribution] in 224 patients with CKD stages 1-3 due to macroalbuminuric, non-diabetic, hypertension-associated nephropathy.

Results

Because Pcit, UcitV, UcitV/Pcit, and PTCO2 each directly associated with eGFR (p<0.01) and because H+ retention inversely associated with eGFR (p<0.01), we adjusted reported associations for eGFR. PRAL associated directly with 8h NAE (p<0.01, R2=0.05) and inversely with UcitV/Pcit (p=0.03, R2=0.13) but not with PTCO2 (p=0.15), H+ retention (p=0.85), UcitV (p=0.21) or Pcit (p=0.49). PTCO2 associated inversely with H+ retention (p<0.01, R2=0.06) but not with 8h NAE (p=0.14), UcitV (p=0.59), Pcit (p=0.11) or with UcitV/Pcit (p=0.79). By contrast, H+ retention associated inversely with UcitV (p<0.01, R2=0.55), Pcit (p<0.01, R2=0.52) and with UcitV/Pcit (p<0.01, R2=0.20) but not with 8h NAE (p=0.12).

Conclusion

Ongoing dietary acid intake assessed by PRAL associated inversely with UcitV/Pcit, although quantitatively less than did H+ retention (R2 0.13 vs. 0.20), but did not associate with the remaining measures of citrate homeostasis. By contrast, steady-state acid-base status assessed by H+ retention associated inversely with each measure of citrate homeostasis. The data show that steady-state acid-base status is a more important determinant of UcitV than dietary acid intake and support continued exploration of UcitV as a biomarker of underlying H+ retention in CKD.