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

email@asn-online.org

202-640-4660

The Latest on X

Kidney Week

ASN / Education & Meetings / Kidney Week /

Please note that you are viewing an archived section from 2020 and some content may be unavailable. To unlock all content for 2020, please visit the archives.

Abstract: PO0470

Lower Urine Citrate Excretion Associated with Advanced CKD Stage Is Mediated by Reduced Plasma Citrate and Decreased Kidney Citrate Clearance

Session Information

Category: CKD (Non-Dialysis)

  • 2101 CKD (Non-Dialysis): Epidemiology, Risk Factors, and Prevention

Authors

  • Goraya, Nimrit, Texas A&M University College Station, College Station, 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 citrate excretion (UcitV) might be a biomarker of covert acid (H+) retention in patients with CKD but without metabolic acidosis and so mechanisms that mediate UcitV differences among patients with CKD would help assessment of its biomarker utility. Because longitudinal eGFR decreases in patients with CKD associated with decreasing UcitV (Goraya, et al. AJP 317:F502, 2019), we examined cross-sectional differences in UcitV across CKD stages and mechanisms that mediate such differences.

Methods

We measured 8-hour UcitV (8h UcitV), plasma citrate concentration (Pcit), and kidney citrate clearance citrate (UcitV/Pcit) in 52 patients with CKD 1 (eGFR=99.5±7.7 ml/min/1.73 m2), 120 with CKD 2 (eGFR=73.4±6.1 ml/min/1.73 m2), and 52 with CKD 3 (eGFR=40.1±7.6 ml/min/1.73 m2) with macroalbuminuric, non-diabetic, hypertension-associated nephropathy. We assessed ongoing dietary H+ intake as potential renal acid load (PRAL) and steady-state acid-base status with plasma total CO2 (PTCO2) and H+ retention, the latter 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 weight HCO3 apparent space of distribution.

Results

Although PRAL was not different among CKD 1, CKD 2, and CKD 3 groups (62.4±11.9, 62.9±14.7, and 65.2±7.9 mmol/day, respectively, p=0.47), PTCO2 was progressively lower (26.4±0.7, 25.9±0.6, and 21.6±1.9 mM, respectively, p<0.01) and H+ retention progressively higher (3.9±12.9, 18.2±14.0, and 25.1 ±13.4 mmol, respectively, p<0.01) with advancing CKD stage. 8h UcitV was progressively lower with advancing CKD stage (1.14±0.03, 1.00±0.25, and 0.86±0.10 mmol/1.73m2, respectively, p<0.01) as was Pcit (0.16 ± 0.01, 0.15 ± 0.02, and 0.14 ± 0.01 mM, respectively, p<0.01) and UcitV/Pcit (0.015 ± 0.001, 0.014 ± 0.003, and 0.013 ± 0.001 ml/min/1.73 m2, respectively, p<0.01).

Conclusion

Cross-sectional advanced CKD stage was associated with greater H+ retention and lower UcitV, the latter mediated by lower Pcit and lower UcitV/Pcit. The data support that reduced UcitV associated with decreased eGFR reflects underlying H+ retention with reduced body citrate stores and increased citrate conservation through reduced kidney citrate clearance.