Higher salt intake ups vascular damage markers

A high intake of sodium over a long period of time is associated with increases in serum uric acid and urine albumin excretion, both of which are considered markers of vascular endothelial damage [1]. These are the findings of a new study published online June 18, 2012 in Circulation.

"Serum uric acid and urine albumin excretion tend to rise over time, as people get older," lead author Dr John P Forman (Brigham and Women's Hospital, Boston, MA), a nephrologist, told heartwire . "But what we found in this cohort of people, without hypertension at baseline, is that these values rise more quickly in the people who eat the most sodium."

He likens this to a kind of "positive feedback loop" and says this would argue against the stance of those people who say that altering sodium intake at the population level is not necessary because only around a third of people are salt sensitive. "Maybe if you're on a high-salt diet for long enough you become one of those people who are salt sensitive and then you develop hypertension. This study supports the view that populations should reduce sodium intake," he says. However, he stresses that this theory is, until confirmed, "speculative."

First link between higher sodium intake and rising uric acid
Forman and colleagues prospectively analyzed the associations between sodium intake and the change in serum uric acid (n=4062) and urinary albumin excretion (n=4146) among participants of the Dutch Prevention of Renal and Vascular End Stage Disease (PREVEND) study.

They also examined the association of sodium intake with the incidence of hypertension among 5556 participants. Median follow-up was 6.4 years.

After multivariate adjustment, each 1-g higher sodium intake was associated with a 1.2-µmol/L increase in serum uric acid (p=0.01) and a 4.6 mg/day increase in urinary albumin excretion (p<0.001).

The relationship between sodium intake and incident hypertension varied according to serum uric acid and urinary albumin excretion.

For each 1-g higher sodium intake, the adjusted hazard ratio for developing hypertension was 0.98 among those in the lowest tertile of uric acid and 1.09 among those in the highest tertile. Corresponding HRs were 0.99 among those with the lowest urinary albumin excretion (<10 mg/day) and 1.18 among those with the highest (>15 mg/day).

The researchers say their study has a number of strengths, including the fact that sodium and albumin were ascertained via multiple 24-hour urinary specimens. There were also limitations, however, including the fact that most of the participants were white, which restricts the generalizability of the findings, they point out.

Forman and colleagues say that, to the best of their knowledge, this is the first time that the relation between sodium intake and increasing serum uric acid has been demonstrated. But the effect of sodium intake on albumin excretion has been observed before, they note, in several clinical trials and large observational studies.

Does a positive feedback loop explain so-called salt sensitivity?
"Those who had a high salt intake compared with low salt intake were at a higher risk of hypertension if they had higher levels of urine albumin excretion and serum uric acid," Forman explains.

"But in the people in the lowest categories of urine albumin excretion and serum uric acid there was no association between sodium intake and the risk of developing high blood pressure, suggesting--although this is purely speculative--that it's the people who have some sort of level of vascular damage that, if they eat a high-salt diet, are at a high risk of developing hypertension.

"If you take both of those findings and put them together and you think of the lifetime of an individual, you could extrapolate and say that maybe eating a very high-salt diet is leading first to vascular damage, which we can see by an increase in the blood and urine levels of markers, and then if you continue the high-salt diet, that can lead to hypertension."

However, he stresses, that this theory needs to be tested in other prospective cohorts and, if possible, in randomized trials.

And while Forman says "It's too far away to talk about screening people for endothelial dysfunction, so that we know whether or not they should eat a low-salt diet," he points out that guidance on salt intake already exists for many individuals.

"For example, the AHA recommends a very low-sodium diet for African Americans, those over 50, and those with hypertension or diabetes. These individuals are more likely to fit into the higher levels of urine albumin excretion and serum uric acid classes and are more likely to have endothelial damage."

But he also stresses "that for everyone else in the population, they still recommend a low-sodium diet, much lower than we are eating in general."

Source: http://www.medscape.com/viewarticle/765937?sssdmh=dm1.795387&src=nldne