Sodium bicarbonate administration for patients with CKD and concurrent metabolic acidosis
Despite advances in the available treatments for patients with chronic kidney disease (CKD), concerns for the development of metabolic acidosis (MA) remain due to its associated increased risk for several complications, particularly deterioration in CKD, cardiovascular (CV) disease and mortality. The use of sodium bicarbonate to treat concurrent MA in patients with CKD has not been specifically studied, nor its effects on other biomarkers, such as muscle mass and intact parathyroid hormone (iPTH).
Through a meta-analysis of randomised controlled trials (RCTs), Yang and colleagues sought to primarily determine the impact of oral sodium bicarbonate on estimated glomerular filtration rate (eGFR) in patients with concurrent MA and CKD. Additionally, they aimed to further characterise its effect on other biomarkers and outcomes; namely baseline systolic blood pressure (SBP), treatment-associated adverse events (e.g. all-cause mortality, hospitalisation rates, CV events), changes in body weight, 24-hour urine sodium excretion, serum bicarbonate, albumin, potassium, calcium, phosphate, iPTH level and mid-arm muscle circumference.
A total of 14 RCTs comprising 2037 patients with CKD (defined as a persistently reduced eGFR <60 mL/min/1.73 m2) and MA who received oral sodium bicarbonate vs placebo/standard of care/rescue therapy over various follow-up periods were included. It is important to note that the investigators chose to exclude patients with oedema-related diagnoses or symptoms, including overt heart failure, but included patients with both subclinical and clinical MA (i.e. a total serum carbon dioxide level <24 mEq/L) previously shown to safely receive sodium bicarbonate and potentially benefit from it. Most of the studies included focused upon patients ≤65 years, predominantly male, with CKD stages 3 to 5. The dosages of sodium bicarbonate ranged from 1.82 to 11.34 g/day.
The results showed statistically significant improvements favouring sodium bicarbonate administration with regards to eGFR (standardised mean difference [SMD], 0.33; 95% confidence interval [CI], 0.03–0.63; P=0.03), particularly in Asian populations; hospitalisation rate (odds ratio, 0.37; 95% CI, 0.25–0.55; P<0.001); and mid-arm muscle circumference (SMD, 0.23; 95% CI, 0.08–0.38; P=0.003; I2<0.001). However, there was an associated risk of elevated systolic BP in the sodium bicarbonate group vs the control group (SMD, 0.10; 95% CI, 0.01–0.20; P=0.03). There was no significant difference in all-cause mortality.
These findings suggest that sodium bicarbonate supplementation may provide benefit, despite the associated elevation in blood pressure. The authors do concede that due to the risk of bias evident in the absence of double-blinding and inconsistent definitions, further research is needed to verify these findings.
The full article can be read here.
