Treatment Blocks Kidney Disease In Rat Experiment
NEW YORK (AP) _ A disease that can cause kidney failure has been arrested in rats by an experimental drug, raising hopes for a new human therapy, researchers said today.
The disease, called glomerulonephritis, strikes perhaps 100,000 Americans a year, researcher Dr. Wayne Border said.
A medication like the one used in the experiment may someday be able to stop the disease’s progression, so patients wouldn’t need dialysis or transplants, he said.
Such a treatment may also work for a similar kidney complication of diabetes and high blood pressure, Border, a kidney specialist at the University of Utah School of Medicine, said in an interview.
The rat study was published today in the British journal Nature.
The work raises ″exciting possibilities″ in a new line of research, said Dr. Ira Greifer, professor of pediatrics and nephrology at the Albert Einstein College of Medicine and Montefiore Medical Center in New York.
Existing drugs don’t always work and can produce major side effects, he said.
But it will take more research to determine what the new approach means for treating human disease, cautioned Dr. Lawrence Agodoa of the National Institute of Diabetes, Digestive and Kidney Diseases.
Glomerulonephritis (pronounced glo-MER-u-low-neh-FRI-tis) is an inflammatory process that can destroy ball-shaped kidney structures called glomeruli. The structures help remove wastes from the bloodstream. If destruction is extensive enough, wastes can accumulate in the bloodstream and cause death.
Glomerulonephritis can appear by itself or in conjunction with a chronic disease called lupus, strep throat or a variety of infections.
The researchers gave rats a form of glomerulonephritis by making the rats’ disease-fighting immune system attack the glomeruli. Although the cause of the human disease is not well understood, such an attack frequently appears to play a key role, they said.
Then they injected some of the rats with proteins called antibodies that would seek out and latch onto a natural substance called transforming growth factor beta. Previous studies suggested that this substance stimulates the glomeruli to produce a protein meshwork that leads to destructive scarring.
The scientists reasoned that if the antibodies could bind to the growth factor and disable it, the production of the meshwork might stop.
Agodoa said nobody has yet shown that the growth factor plays a role in human glomerulonephritis.
Greifer said he doubted the work would apply to kidney scarring caused by high blood pressure, because that scarring comes from a different process.
Other researchers in the study were Selya Okuda of the Utah medical school, Erkki Ruoslahti and Lucia Languino of the La Jolla Cancer Research Foundation in La Jolla, Calif., and Michael Sporn of the National Cancer Institute.