High Dietary Phosphate Boosts Blood Pressure in Healthy People

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High dietary phosphate levels are known to be harmful for patients with advanced kidney disease. Now an abstract presented at ASN Kidney Week 2017 suggests that high phosphate diets also may have detrimental effects on the cardiovascular health of healthy people.

In patients with advanced kidney disease there is evidence that a high-phosphate diet is associated with worse cardiovascular disease, said Kevin J. Martin, MD, a professor of internal medicine and director of the division of nephrology at St. Louis University, who was not involved in the study. In fact, patients are often urged to limit phosphorous in their diets, a tricky task given that food makers are not required to list this popular preservative on labeling, Martin explained. Phosphorous binding agents are also sometimes used, but he noted more evidence from clinical trials is needed to determine their effects (Cannata-Andía JB and Martin KJ. Nephrol Dial Transplant 2016; 31:541–7).

Epidemiological studies have also found higher dietary phosphate intake and blood phosphate concentration are linked to worse cardiovascular outcomes, noted one of the abstract’s authors, Reto Krapf, MD, of the University of Basel in Switzerland. This is particularly concerning because phosphate levels appear to be increasing in Western diets.

To determine if increased dietary phosphate might have cardio-toxic effects, Krapf and his colleagues conducted a prospective study in which 20 healthy young people with normal kidney function were randomly assigned to a high- or low-phosphate diet for 11 weeks. At 6 weeks, both groups received a 600,000 U dose of vitamin D3.

Patients on the high-phosphate diet experienced increased systolic (plus 4.1) and diastolic blood pressure (plus 3.2) compared with baseline and with the low-phosphate group. The average heart rate in this group also increased by 4 beats per minute. Plasma renin/aldosterone concentrations and 24-hour urinary excretion rates of sodium, aldosterone, and free cortisol were comparable between the two groups. The vitamin D dose had no effect on blood pressure or pulse rate in the high-phosphate group, but it increased phosphate levels in the low-phosphate diet group.

At follow-up visits 2 months after the diet ended, the elevated blood pressures and pulse rate in the high-phosphate group returned to normal.

“By identifying the phenomenon of dietary phosphate–induced hypertension and acceleration of mean heart rate, we provide at least one important mechanism that explains the increased cardiovascular morbidity and mortality associated with increased phosphate intake,” Krapf said. “Our study also identifies increased sympathetoadrenergic activity as the most likely cause of phosphate-induced hypertension.”

Martin said the study was well done and extends the evidence regarding the vascular toxicity of high-phosphate diets into an otherwise healthy population.

“Just a high-phosphate diet is enough to raise blood pressure; that was kind of interesting,” Martin said. He suggested it might help organizations like the National Kidney Foundation convince the US Food and Drug Administration to require phosphate labeling.

Krapf suggested that limiting phosphate in the diet might be a good step to protect kidney health.

“Hypertension is a very important cause of kidney disease and high phosphate intake or experimentally administered high phosphate loading has been shown to cause kidney disease and progressive renal failure,” he said. “Thus, limiting phosphate intake in humans—both with normal and decreased renal function—may protect the kidneys both directly [by decreasing phosphate load] and indirectly [by decreasing blood pressure].”

“Effect of Dietary Phosphate Intake on Blood Pressure in Healthy Humans” (Abstract SA-OR027)