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Abstract: FR-PO273

Effects of Treatment of Metabolic Acidosis in CKD: A Systematic Review and Meta-Analysis

Session Information

Category: Fluid and Electrolytes

  • 902 Fluid and Electrolytes: Clinical

Authors

  • Navaneethan, Sankar D., Baylor College of Medicine, Sugar Land, Texas, United States
  • Buysse, Jerry M., Tricida, Inc, South San Francisco, California, United States
  • Shao, Jun, Tricida, Inc., South San Francisco, California, United States
  • Parsell, Dawn, Parsell and Otto Consulting, Inc., Cedar Park, Texas, United States
  • Bushinsky, David A., University of Rochester Medical Center, Rochester, New York, United States
Background

Metabolic acidosis is an important risk factor for disease progression in chronic kidney disease (CKD) that also has significant adverse effects on muscle and bone. We conducted a systematic review and meta-analysis to evaluate the benefits and risks of treatment of metabolic acidosis with oral alkali supplements or reduction of acid load with dietary intervention.

Methods

We searched MEDLINE, Embase, and Cochrane Central Register of Controlled Trials for clinical trials (with a control group) of oral alkali supplementation or low acid-producing dietary intervention in stage 3-5 CKD patients for a minimum of 4 weeks. Data were pooled in a meta-analysis with results expressed as weighted mean difference (intervention versus control; WMD) for continuous outcomes and relative risk (RR) for categorical outcomes with 95% confidence intervals (CI) using a random effects model.

Results

Fourteen clinical trials were included (n=1810 participants). Both oral alkali supplementation and dietary intervention increased serum bicarbonate levels (Table). Treatment resulted in a slower decline in eGFR and a reduction in urinary albumin excretion, along with a reduction in the risk of progression to ESRD (4 trials; n=434; RR 0.32, 95% CI 0.18, 0.56). Important exclusions noted in the oral alkali studies were CKD patients with sodium-sensitive comorbidities (edema, heart failure, uncontrolled hypertension). Oral alkali supplementation was associated with significantly increased urinary sodium excretion, and trends of elevated diastolic blood pressure and increased antihypertensive therapy, although these trends were not statistically significant. Dietary intervention was associated with a significant reduction in systolic blood pressure. Included studies were of moderate quality.

Conclusion

In patients with CKD and metabolic acidosis, an increase in serum bicarbonate concentration induced either by oral alkali supplementation or reduction in dietary acid intake slows the rate of kidney function decline and reduces urinary albumin excretion.

Funding

  • Commercial Support