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Abstract: SA-OR035

Urine Citrate Excretion Reliably and Non-Invasively Identifies Acid Retention in CKD 2 Patients without Metabolic Acidosis

Session Information

Category: Fluid and Electrolytes

  • 902 Fluid and Electrolytes: Clinical


  • Goraya, Nimrit, Baylor Scott and White Health , Temple, Texas, United States
  • Simoni, Jan, Texas Tech University Health Sciences Center, Lubbock, Texas, United States
  • Sager, Lauren N., Baylor Scott & White, Temple, Texas, United States
  • Madias, Nicolaos E., Tufts University School of Medicine, Boston, Massachusetts, United States
  • Wesson, Donald E., Baylor Scott and White Health and Wellness Center, Dallas, Texas, United States

Dietary acid (H+) reduction slows eGFR decline in CKD stage 2 (eGFR=60-89 ml/min/1.73 m2, CKD 2) patients without metabolic acidosis (conventionally defined as plasma total CO2 <22 mM) (Mahajan et al, Kid Int, 2010) but who have H+ retention identified using cumbersome and invasive methods. Earlier studies from this laboratory supported the potential utility of urine citrate excretion to non-invasively identify H+ retention in such patients but its reliability to do so was not assessed.


We measured H+ retention and 8-hour urine citrate excretion (UcitrateV) in macroalbuminuric, non-diabetic CKD 2 (n=40) and CKD stage 1 (eGFR >90 ml/min/1.73 m2, CKD 1, n=26) patients with hypertension-associated nephropathy but without metabolic acidosis (mean plasma total CO2 25.9±0.8 and 26.4±0.6 mM, respectively). H+ retention was measured by comparing observed to the expected increase in plasma [HCO3] in response to retained HCO3 (dose minus UHCO3V) 6 hours after oral NaHCO3 bolus (0.5 mmol/kg bw), assuming 50% body weight HCO3 apparent space of distribution.


H+ retention was higher in CKD 2 than CKD 1 (28.1±9.4 vs. 5.2±12.0 mmol, respectively, p<0.01) but UcitrateV was lower in CKD 2 than CKD 1 (187±40 vs. 335±125 mg, respectively, p<0.01). Overall Pearson correlation for UcitrateV with H+ retention was -0.76 (p<0.001) and a mixed effects regression model showed lower UcitrateV to be strongly predictive of higher H+ retention (p<0.001). Using the 90th percentile of H+ retention in CKD 1 (19.5 mmol) as normal, UcitrateV of 230 mg in CKD 2 patients had sensitivity 93.7%, specificity 62.5%, positive predictive value 90.9%, negative predictive value 71.4%, and an accuracy of 87.5% to predict H+ retention.


Lower UcitrateV reliably identifies CKD 2 patients with higher H+ retention in the absence of metabolic acidosis by acid-base parameters. Because <2% of CKD 2 patients have metabolic acidosis (Shah et al, AJKD, 2009), follow-up studies should further refine this simple, non-invasive method to identify CKD 2 patients who are candidates for dietary H+ reduction which might reduce their risk for nephropathy progression.