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Abstract: SA-OR078

Higher eGFR at Ten Years in CKD Stage 2 Patients Treated with Chronic Oral NaHCO3 Despite No Metabolic Acidosis Is Associated with Prevented Worsening of Underlying Acid Retention

Session Information

Category: CKD (Non-Dialysis)

  • 1901 CKD (Non-Dialysis): Epidemiology, Risk Factors, and Prevention


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

Chronic oral NaHCO3 but not eqimolar NaCl preserves eGFR compared to placebo in CKD stage 2 (eGFR=60-89 ml/min/1.73 m2, CKD 2) patients (Mahajan et al, KI, 2010) without metabolic acidosis (conventionally defined as plasma total CO2 <22 mM). Because amelioration of underlying H+ retention with dietary alkali in experimental CKD models without metabolic acidosis helped preserved GFR (Wesson et al, Kid Int 2010), we explored if eGFR preservation in CKD 2 patients without metabolic acidosis receiving NaHCO3 was associated with amelioration of underlying acid (H+) retention.


We randomized 120 CKD 2 non-diabetic, macroalbuminuric subjects with hypertension-associated nephropathy without metabolic acidosis (plasma total CO2 > 24 mM) to receive 0.5 meq/kg bw/day NaHCO3 (HCO3, n=40), 0.5 meq/kg bw/day NaCl (NaCl, n=40), or to usual care (UC, n=40) and assessed them yearly for 10 years. We measured Cystatin C-based estimated GFR (eGFR) and H+ retention by comparing observed to expected increase in plasma total CO2 in response to retained HCO3 (dose minus UHCO3V) 2 hours after oral NaHCO3 bolus (0.5 mmol/kg bw), assuming 50% body weight HCO3 apparent space of distribution.


Baseline eGFR was not different among groups, was lower than their respective baseline for each group at 10 years, but the 10-year value was higher (p<0.01) in HCO3 (60.3±4.8 ml/min/1.73 m2) than NaCl and UC (52.2±5.8 and 51.4±4.6 ml/min/1.73 m2, respectively). Baseline H+ retention was not different among groups and the 10-year vs. baseline value was not different for HCO3 (15.7±12.6 vs. 18.1±14.87 mmol, p=0.90). By contrast, 10-year H+ retention was higher than baseline in NaCl (27.5±15.2 vs. 19.2±16.7 mmol, respectively, p<0.01) and UC (22.1±11.2 vs. 17.4±9.9 mmol, p<0.01)


Better eGFR preservation in NaHCO3-treated CKD 2 patients without metabolic acidosis was associated with no worsening of underlying H+ retention whereas H+ retention worsened in NaCl and UC with less eGFR preservation. The data support that worsening H+ retention, without metabolic acidosis, contributed to nephropathy progression in CKD. The data suggest that more aggressive NaHCO3 dosing might reduce H+ retention, rather than preserve its level, possibly yielding even greater eGFR protection.