Kidney Week

Abstract: SA-OR035

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

Session Information

• Fluids and Electrolytes: Clinical, Translational, and Acid-Base
  October 27, 2018 | Location: 23A, San Diego Convention Center
  Abstract Time: 05:18 PM - 05:30 PM

Category: Fluid and Electrolytes

• 902 Fluid and Electrolytes: Clinical

Authors

• Goraya, Nimrit, Baylor Scott and White Health , Temple, Texas, United States

Nimrit Goraya, MD

Am a Nephrology Fellowship Program Training Director at Baylor Scott and White, Temple, TX. My core interests include acid-base metabolism with particular interest in metabolic acidosis in Chronic Kidney Disease . My research has been focused on dietary management of metabolic acidosis and to generate tools to aid and help slow CKD progression.

• Simoni, Jan, Texas Tech University Health Sciences Center, Lubbock, Texas, United States

Jan Simoni,

• Sager, Lauren N., Baylor Scott & White, Temple, Texas, United States

Lauren N. Sager,

• Madias, Nicolaos E., Tufts University School of Medicine, Boston, Massachusetts, United States

Nicolaos E. Madias,

• Wesson, Donald E., Baylor Scott and White Health and Wellness Center, Dallas, Texas, United States

Donald E. Wesson,

Background

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.

Methods

We measured H⁺ retention and 8-hour urine citrate excretion (U_citrateV) 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 U_HCO3V) 6 hours after oral NaHCO₃ bolus (0.5 mmol/kg bw), assuming 50% body weight HCO₃ apparent space of distribution.

Results

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 U_citrateV was lower in CKD 2 than CKD 1 (187±40 vs. 335±125 mg, respectively, p<0.01). Overall Pearson correlation for U_citrateV with H⁺ retention was -0.76 (p<0.001) and a mixed effects regression model showed lower U_citrateV 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, U_citrateV 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.

Conclusion

Lower U_citrateV 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.