Mice lacking only one copy of the gene for CD2-associated protein (CD2AP) appear to be significantly more susceptible to kidney disease and failure than normal mice. Moreover, the mutation appears to impair the elimination of proteins that accumulate in the kidney, a previously unidentified process.
The study, which will be published in the May 23 issue of the journal Science, is the first to suggest that proteins normally pass into the kidneys and that kidney disease may result from an inability to draw them back out. It also identifies at least two patients with kidney disease who lack one copy of CD2AP, suggesting that this mutation may be responsible for illness in some humans.
"Most experts believe that kidney disease is caused by an immune response against the kidney," explains principal investigator Andrey S. Shaw, M.D., professor of pathology and immunology at Washington University School of Medicine in St. Louis. "But our evidence suggests that defects that are intrinsic to the kidney also contribute to kidney failure."
Gila Z. Reckess | EurekAlert!
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