Researchers tracked a chain reaction that leads from kidney damage to weakening of the skeleton to increased phosphorous in the blood. They showed that higher phosphorous levels were directly linked to vascular calcification, a stiffening of the smooth muscle cells that line blood vessels. Vascular calcification leads to enlargement of one of the heart's four chambers, increased risk of congestive heart failure, heart attack and several other cardiac problems.
Mice treated with an experimental medication that alleviates the skeletal weakening brought on by kidney damage had normal phosphorous levels and decreased signs of vascular calcification.
"We already have treatments available that can control phosphorous levels in the blood, and those should be very helpful for kidney patients," says senior investigator Keith A. Hruska, M.D., the Ira M. Lang Professor of Nephrology and professor of pediatrics and of cell biology and physiology at Washington University School of Medicine in St. Louis. "The drug we used in the mice and other similar agents can treat both the phosphorous levels and skeletal weakening, and those drugs are just entering initial clinical trials."
The study will appear in the April issue of the Journal of the American Society of Nephrology.
Hruska, who is director of nephrology at St. Louis Children's Hospital, has long been interested in the connections between kidney damage and bone weakening. He and other researchers have uncovered a complex network of links between the skeleton and the kidney. Hormones made in the kidney regulate activity in the skeleton and vice-versa.
Last year, Hruska showed that injections of bone morphogenetic protein-7 (BMP-7) could prevent bone weakening in mice wh
Contact: Michael C. Purdy
Washington University School of Medicine