Higher salt intake may increase risk of CKD, other conditions


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Key takeaways:

  • Adults with a higher self-reported salt intake were more likely to have a diminished eGFR.
  • Participants who reported “always” adding salt had an 11% increased risk for CKD.

A higher frequency of adding salt to food may be associated with an increased risk of chronic kidney disease in the general population, according to a recently published study.

Researchers led by Rui Tang, MS, MPH, of the department of epidemiology at Tulane University in New Orleans, led a trial to “prospectively examine the association of self-reported frequency of adding salt to foods with incident CKD,” they wrote in the report. “The association of high sodium consumption with hypertension has been well established in previous studies. … Although many studies to date have investigated the association of dietary sodium intake with the risk of CKD, most have only included participants who have already received a diagnosis of hypertension, diabetes or other chronic conditions.”

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Participants who reported ‘always’ adding salt had an 11% increased risk for CKD.

Investigators evaluated 465,288 adults (aged 37 to 73 years) from the UK Biobank and who were enrolled from 2006 to 2010 and free of CKD at baseline. Patients were prospectively followed up for diagnosis, and researchers examined data from 2022 to 2023. The UK Northwest Multicenter Research Ethics Committee is a national, population-based cohort study designed to improve the prevention, diagnosis and treatment of various illnesses.

The study aimed to evaluate potential links between adding salt to foods and the risk of incident CKD in a general population. Participants self-reported their frequency of salt addition to foods and were categorized into four groups: “never or rarely,” “sometimes,” “usually” and “always.” The main outcome was incident CKD, identified through diagnostic codes.

During a median follow-up of 11.8 years, researchers found 22,031 incident cases of CKD.

Results showed that patients with a higher self-reported frequency of salt intake were more likely to have a higher BMI and diminished eGFR compared to those with a lower frequency of adding salt. In addition to likely being a current smoker or drinker or having diabetes or cardiovascular disease at baseline, patients with higher salt intake frequency were also more likely to have a higher Townsend Deprivation Index score, a composite measure of deprivation based on unemployment and socioeconomic status.

Participants who reported “sometimes” adding salt to food had a 4% increased risk, those who reported “usually” adding salt had a 7% increased risk and those who reported “always” adding salt had an 11% increased risk for CKD vs. those who “never or rarely” did.

The links were greater in patients with a higher eGFR, lower BMI and lower physical activity.

“These findings suggest that reducing the frequency of adding salt to foods at the table might be a valuable strategy to lower CKD risk,” Tang and colleagues wrote.

BLAME IT ON YOUR BRAIN: SALT AND HYPERTENSION


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While the link between salt and hypertension is well known, scientists until now haven’t understood how high salt intake increased blood pressure. By studying the brains of rats, a team led by Prof. Charles Bourque of McGill’s Faculty of Medicine discovered that ingesting large amounts of dietary salt causes changes in key brain circuits.

“We found that a period of high dietary salt intake in rats causes a biochemical change in the neurons that release vasopressin (VP) into the systemic circulation”, says Bourque who is also a researcher at the The Research Institute of the McGill University Health Centre (RI-MUHC). “This change, which involves a neurotrophic molecule called BDNF (brain-derived neurotrophic factor), prevents the inhibition of these particular neurons by other cells”.

The team’s findings, published today in the journal Neuron, found that high salt intake prevents the inhibition of VP neurons by the body’s arterial pressure detection circuit. The disabling of this natural safety mechanism allows blood pressure to rise when a high amount of salt is ingested over a long period of time.

While the team’s discovery advances the understanding of the link between salt intake and blood pressure, more work is needed to define new targets that could potentially be explored for therapeutic intervention. Among the questions for further research: Does the same reprogramming effect hold true for humans? If so, how might it be reversed?

In the meantime, Bourque says, the message remains: limit dietary salt.