"We still have some mechanical and structural testing to do to prove that the skeletons of these mice are normal, but if this works out and we're able to apply it in humans, we could be on our way to producing a major improvement in the well-being of patients with chronic kidney disease," says 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.
Hruska was principal investigator for the study, which appears in the February issue of the Journal of the American Society for Nephrology. Scientists gave injections of bone morphogenetic protein-7 (BMP-7), a protein involved in both bone and kidney growth, to mice with damaged and removed kidneys. The injections prevented a condition known as adynamic bone disorder (ABD) that leads to weakening and distortion of bone.
"Adynamic bone disorder means that the cells that remodel bones are markedly diminished in number and activity," Hruska explains. "In the past, the skeleton has been viewed as a mostly dead structure, but that's not the case at all. The adult skeleton is a very active tissue that is continually remodeling."
ABD is the second type of bone weakening related to kidney problems that scientists have identified. In the first, secondary hyperparathyroidism, patients have weakened bones like in ABD, but also have abnormal blood levels of the hormone produced by the parathyroid gland and several other important chemicals.
Hruska suspects secondary hyperparathyroidism may be a failed attempt to compensate for ABD, which first emerged about 15 years ago when scientists began using drugs to suppress parathyroid hormone levels in kidney patients.
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Contact: Michael C. Purdy
purdym@msnotes.wustl.edu
314-286-0122
Washington University School of Medicine
6-Feb-2004