Key result
High salt accelerates age-induced BP and kidney damage in animals, with albuminuria preceding BP changes.
Why the study?
Direct evidence of the longitudinal cardiovascular and renal changes that occur with aging, and the influence of dietary sodium on these age-associated alterations, is scarce.
Does increasing dietary sodium intake accelerate age-induced changes in blood pressure and albuminuria in an animal model?
Does increasing dietary sodium intake accelerate age-induced changes in blood pressure and albuminuria in an animal model?
Increasing dietary salt accelerates age-induced cardiorenal dysfunction in an animal model, with albuminuria preceding blood pressure changes, suggesting its potential utility as a prognostic biomarker for future hypertension.
Answers are grounded in this paper and cite their sources.
Salt acceleration of age-related BP and renal injury in animals is hypothesis-generating; leaves open albuminuria as early prognostic marker in humans.
BACKGROUND: Dietary sodium is a well-known risk factor for cardiovascular and renal disease; however, direct evidence of the longitudinal changes that occur with aging, and the influence of dietary sodium on the age-associated alterations are scarce. METHODS: ) salt diet. We assessed 1) the longitudinal trajectories for two markers of cardiovascular and renal dysfunction (blood pressure (BP) and albuminuria), as well as hormonal changes, and 2) end-of-study cardiac and renal parameters. RESULTS: The effect of aging on BP and kidney damage did not reach significance levels in the LS group; however, relative to baseline, there were significant increases in these parameters for animals maintained on NS and HS diets, starting as early as month 7 and month 5, respectively. Furthermore, changes in albuminuria preceded the changes in BP relative to baseline, irrespective of the diet. Circulating aldosterone and plasma renin activity displayed the expected decreasing trends with age and dietary sodium loading. As compared to LS - higher dietary sodium consumption associated with increasing trends in left ventricular mass and volume indices, consistent with an eccentric dilated phenotype. Functional and molecular markers of kidney dysfunction displayed similar trends with increasing long-term sodium levels: higher renovascular resistance, increased glomerular volumes, as well as higher levels of renal angiotensin II type 1 and mineralocorticoid receptors, and lower renal Klotho levels. CONCLUSION: Our study provides a timeline for the development of cardiorenal dysfunction with aging, and documents that increasing dietary salt accelerates the age-induced phenotypes. In addition, we propose albuminuria as a prognostic biomarker for the future development of hypertension. Last, we identified functional and molecular markers of renal dysfunction that associate with long-term dietary salt loading.
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Katayama et al. (2023) studied Cardiovascular and renal dysfunction. Normal and high dietary sodium vs. Low salt diet was evaluated on Longitudinal trajectories for blood pressure and albuminuria. Increasing dietary salt accelerated age-induced increases in blood pressure and kidney damage in animals, with albuminuria changes preceding blood pressure changes irrespective of diet.
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