NEW YORK (AP) _ A kidney disease that strikes an estimated 100,000 Americans a year has been blocked in rats by an experimental drug that could become a new alternative to transplants or dialysis, a researcher says.

Such a treatment for the disease - glomerulonephritis - also may work for a similar kidney complication of diabetes and high blood pressure, said the researcher, Dr. Wayne Border, a kidney specialist at the University of Utah School of Medicine.

Border reports the work in Thursday's issue of the British journal Nature with Selya Okuda at the 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.

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.

Currently used drugs do not 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, director of clinical studies in the divison of kidney, urologic and hematologic diseases at the National Institute of Diabetes, Digestive and Kidney Diseases.

Glomerulonephritis (pronounced glo-MER-ulo-ne-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.

The disease 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 animals' 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.

They then 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 prouce 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.

The treatment ''clearly protected from the accumulation of the vast amount of matrix which occurs as part of the disease process,'' Border said in a telephone interview.

Agodoa said nobody has yet shown that the growth factor plays a role in human glomerulonephritis. Scientists must also see if the experimental treatment works when the kidney scarring is produced by other means in animals, he said.

Greifer said he doubted the work would apply to kidney scarring caused by high blood pressure, because that scarring comes from a different process.