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Mouse model reveals potential way to reduce cardiac deaths in kidney patients

ose kidneys had been damaged or removed.

For the new study, researchers worked with a mouse model of metabolic syndrome, a condition common among patients with chronic kidney disease that includes symptoms such as obesity, high blood pressure and insulin resistance. The condition, which is rapidly increasing in both adults and children, is also associated with higher risks of diabetes and heart disease.

The mice develop metabolic syndrome as a result of both a genetic modification and a high-fat, high-cholesterol diet. To simulate chronic kidney disease, scientists damaged or removed part of the kidney. This led to a shutdown of cells that regularly dismantle and rebuild bones, causing vascular calcification.

The body normally takes minerals like calcium and phosphorous circulating in the bloodstream and deposits them in the bones during bone reconstruction. With those processes shut down, scientists theorized, the bloodstream levels of minerals increase, raising pressure to deposit them elsewhere.

Hruska and his colleagues first showed that injection of BMP-7, previously shown to stop the bone disorder, also stopped vascular calcification. In another group of experimental mice, injections of a substance that binds to compounds with phosphorous but has no effect on the skeleton also stopped vascular calcification, proving that phosphorous was the key link.

"Serum phosphorous is a direct stimulus to the smooth muscle cells that line blood vessels, causing them to take on characteristics very similar to osteoblasts, the cells that form bone," Hruska explains.

The changed smooth muscle cells can deposit minerals outside their membranes, dramatically decreasing the flexibility of blood vessels and increasing the work the heart has to do to create a pulse.

"Vascular stiffness happens to patients with end-stage kidney failure when they go on dialysis, and it leads to many dangerous cardiovascular complications,
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Contact: Michael C. Purdy
purdym@wustl.edu
314-286-0122
Washington University School of Medicine
29-Mar-2005


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