According to study co-author Kumar Sharma, M.D., director of the Center for Diabetic Kidney Disease at Thomas Jefferson University in Philadelphia and professor of medicine at Jefferson Medical College of Thomas Jefferson University, more than 40 percent of patients with end-stage chronic kidney disease also have diabetic nephropathy. While diabetic nephropathy affects approximately one in three people with type 1 and type 2 diabetes, how diabetes damages the kidneys is poorly understood.
Dr. Sharma, along with Erwin Bttinger, M.D., professor of medicine and pharmacology and biological chemistry at Mount Sinai School of Medicine in New York, and their co-workers looked at kidney samples from mice and people with and without diabetes and looked at the effects of high glucose on the kidney cells.
The researchers found that a protein called CD36 was present in a specific cell type called the proximal tubular epithelial cell in human diabetic kidney disease. In humans, the cells seem to be involved in a self-directed cell death or apoptosis in diabetic kidney disease.
"We think CD36 might be a switch that is turned on in the human condition, and
might be one of the reasons these cells die in human disease and start a cascade of progressive kidney failure," Dr. Sharma explains. "If we can develop compounds to block CD36, it could potentially be a clinical intervention.
"Our thinking is completely novel that CD36 is a key player in causing
progressive diabetic kidney disease," he says. "W