Key result
Diet-dependent acid load, estimated by urinary potential renal acid load, was inversely associated with mean arterial pressure (β -0.11) in healthy postmenopausal women.
Why the study?
It was not well determined whether the association between higher sodium intake and higher blood pressure is stronger with diet-dependent acid load, or how it differs by hypertension status.
Is diet-dependent acid load (UPRAL) associated with mean arterial pressure in postmenopausal women?
Cohort (n=170)
Randomized to placebo or KHCO3 (original trial)
No
Is diet-dependent acid load (UPRAL) associated with mean arterial pressure in postmenopausal women?
Lower urinary potential renal acid load (UPRAL) is independently associated with lower mean arterial pressure in normotensive postmenopausal women, suggesting diet-dependent acid load plays a role in blood pressure regulation.
Supports hypothesis that lower diet acid load relates to lower MAP in postmenopausal women; leaves open causality and practice implications.
Higher sodium (Na + ) intake is associated with higher blood pressure (BP). Whether this relationship is stronger with diet-dependent acid load (DAL) and in patients diagnosed with hypertension or normal BP is not well determined. We studied 170 postmenopausal women randomized to receive potassium bicarbonate or placebo for 36 months, after which 24-hour urine and arterialized blood samples were collected. We investigated the association between DAL estimated as urinary potential renal acid load (UPRAL) and mean arterial pressure (MAP) using a mixed-effects model, adjusting for age, anthropometrics, creatinine clearance, and treatment. Adjusted regression estimates for changes in Na + and UPRAL on MAP after 12 months of follow-up were calculated, and further adjustments were made for changes in potassium (K + ) and body mass index (BMI). MAP was inversely associated with UPRAL (β [95% confidence interval]: –0.11 [–0.25, –0.001]). There was an effect modification by hypertension (p-interaction = 0.04); MAP decreased significantly in normotensives, but the association was not significant in hypertensives. A decrease of 0.70 mm Hg in MAP [0.13, 1.69] per 50 mmol/24 hour reduction in Na + was noted when the model was adjusted for change in K + . Our results with UPRAL exhibited a stronger dose–response for MAP, which remained significant after adjusting for BMI. UPRAL was independently associated with MAP even after adjusting for potential confounders, and the data showed that this association was more pronounced in normotensive patients. Novelty: First longitudinal study on the association of UPRAL and MAP. Association was a more robust relationship than that between U [Na + /K + ] ratio and MAP. UPRAL may play a significant role in the pathogenesis of primary hypertension.
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Banerjee et al. (2021) conducted a cohort in Healthy postmenopausal women (n=170). Urinary potential renal acid load (UPRAL) vs. Lower UPRAL was evaluated on Mean arterial pressure (MAP) (β -0.11, 95% CI -0.25, -0.001, p=0.02). Diet-dependent acid load, estimated by urinary potential renal acid load, was inversely associated with mean arterial pressure (β -0.11) in healthy postmenopausal women.
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