Key result
Oral sodium bicarbonate supplementation over 8 weeks did not increase systolic blood pressure measured by 24h-ABPM compared to rescue therapy in patients with chronic kidney disease.
Why the study?
Additional sodium loading from sodium bicarbonate treatment could worsen arterial hypertension in patients with CKD, an effect that has been under-studied in prospective trials.
Does high-dose oral sodium bicarbonate increase 24-hour ambulatory blood pressure in patients with chronic kidney disease and metabolic acidosis?
RCT (n=47)
Open-label
Yes
No
Does high-dose oral sodium bicarbonate increase 24-hour ambulatory blood pressure in patients with chronic kidney disease and metabolic acidosis?
Answers are grounded in this paper and cite their sources.
Sodium bicarbonate supplementation over 8 weeks did not significantly increase blood pressure measured by 24h-ABPM in patients with CKD and metabolic acidosis.
Background: Sodium bicarbonate supplementation is a mainstay in the treatment of metabolic acidosis in patients with chronic kidney disease (CKD). Recent studies showed reduction of progression of CKD and reduced all-cause mortality. However, additional sodium loading could worsen arterial hypertension, a well-known contributor to progression of CKD. This patient-relevant and economically negative side effect is under-studied in prospective studies up until now. Objective: The aim of this study was to analyze the effect of sodium bicarbonate treatment on arterial blood pressure at baseline and after 8 weeks. Methods: The SoBic study is an ongoing randomized controlled trial, in which patients with CKD receive either a high dose of oral sodium bicarbonate or a rescue treatment, if necessary. We used standardized office blood pressure and 24-hour ambulatory blood pressure monitoring (24h-ABPM). Regression models were adjusted for estimated glomerular filtration rate and change of antihypertensives. Results: 47 subjects were enrolled and the mean age was 57 (±14.6) years and 18 (38%) were female. In 43 randomized subjects with sufficiently performed 24h-ABPM neither systolic 24h-ABPM (2.522; 95%CI: −2.364, 7.408; mmHg) nor diastolic 24h-ABPM (0.868; 95%CI: −2.411, 4.147; mmHg) was affected by study group allocation. When looking at the effect of individual sodium bicarbonate dose on 24h-ABPM, the fully adjusted model suggested an increase of 0.047 (95%CI: −0.026, 0.119) mmHg by each mg/kg per day increase of sodium bicarbonate dose. Conclusion: Sodium bicarbonate supplementation over 8 weeks did not significantly increase blood pressure measured by 24h-ABPM in CKD patients. Trial Registration: EUDRACT Number: 2012-001824-36; 12/07/2012 ( https://www.clinicaltrialsregister.eu ).
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Gaggl et al. (2021) conducted an RCT in Chronic Kidney Disease and Metabolic Acidosis (n=47). Oral sodium bicarbonate vs. Rescue therapy (target serum HCO3- 20 ± 1 mmol/L) was evaluated on Change in systolic 24-hour ambulatory blood pressure from baseline to week 8 (MD 2.522, 95% CI -2.364 to 7.408, p=0.314). Oral sodium bicarbonate supplementation over 8 weeks did not increase systolic blood pressure measured by 24h-ABPM compared to rescue therapy in patients with chronic kidney disease.
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