Kidney Week

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

• New Considerations for Renoprotection Clinical Trials
  October 27, 2018 | Location: 1B, San Diego Convention Center
  Abstract Time: 04:30 PM - 04:42 PM

Category: CKD (Non-Dialysis)

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

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,

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

Donald E. Wesson,

Background

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.

Methods

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 U_HCO3V) 2 hours after oral NaHCO₃ bolus (0.5 mmol/kg bw), assuming 50% body weight HCO₃ apparent space of distribution.

Results

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)

Conclusion

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.