The estimated 19 million Americans living with chronic kidney disease (CKD) face a high risk of death from cardiovascular disease. Recent studies have shown that a main source of this cardiovascular risk is CKD patients' high levels of blood phosphate.
Now researchers at Washington University School of Medicine in St. Louis have demonstrated that high blood phosphate directly stimulates calcification of blood vessels and that phosphate-binding drugs can decrease vascular calcification. That means drugs that reduce phosphate levels could help protect CKD patients from cardiovascular disease, according to the authors of the study, which is available online in advance of print publication in the Journal of the American Society of Nephrology.
"One of the kidney's functions is to help maintain a constant balance of phosphate in the bloodstream," says senior author Keith A. Hruska, M.D., director of the Division of Pediatric Nephrology and professor of pediatrics, of medicine and of cell biology and physiology. "When kidney failure occurs, an excess of serum phosphate develops. It turns out that high phosphate serves as a signal that stimulates cells within blood vessel walls to become bone-forming cells and to deposit calcium crystals. That produces vascular stiffness that is a cause of cardiovascular mortality."
Phosphate-binding drugs are already on the market, and based on evidence in this study and others like it, the Food and Drug Administration has recently decided to extend the label of such drugs. As a result, calcium acetate (PhosLo), sevelamer (Renagel) and lanthanum carbonate (Fosrenol) will be labeled to indicate they are approved for treatment of high serum phosphate levels in patients with CKD.
Hruska, Suresh Mathew, M.D., instructor in pediatrics, and colleagues studied mice with CKD and atherosclerosis calcified plaques in the arteries. They gave the mice phosphate-binding agents, which prevent phosphate in th
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| Contact: Gwen Ericson ericsong@wustl.edu 314-286-0141 Washington University School of Medicine Source:Eurekalert |