From Our 2008 Archives
Rituximab Promotes Healing in Common Kidney Disease
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FRIDAY, Aug. 15 (HealthDay News) -- The drug rituximab may significantly reduce kidney damage in people with a common form of kidney disease called membranous nephropathy, believed to be caused by autoimmune reactions against the kidney.
The disease, characterized by large amounts of protein in the urine, leads to impaired kidney function that may eventually require dialysis or a transplant.
Rituximab may be able to heal the damage caused by membranous nephropathy in some patients, according to a new study. The drug, originally developed as a cancer treatment for people with B cell lymphoma, selectively depletes B lymphocytes, cells that produce kidney-damaging autoantibodies.
The study included 50 patients with membranous nephropathy who were treated with rituximab. Ten of the patients eventually achieved complete remission of their disease. Kidney biopsies of seven of those 10 patients showed that deposits of autoantibodies eventually disappeared or were almost entirely reabsorbed, and there was significant healing in the kidneys.
The study will be published in the November issue of the Clinical Journal of the American Society of Nephrology.
"This represents the first demonstration that kidney injury in membranous nephropathy can regress after selective depletion of B cells. Thus, the present data provide a strong rationale for using rituximab to treat patients with membranous nephropathy," wrote Dr. Piero Ruggenenti, of the Negri Bergamo Laboratories in Italy, and colleagues.
The findings suggest that the functional and biological problems associated with membranous nephropathy can be reversed with a safe and selective drug, they concluded.
"Whether this may apply to other (similar kidney conditions) and may translate into long-term protection from renal function loss and the potentially life-threatening complications remains to be established," the researchers wrote.
-- Robert Preidt
SOURCE: American Society of Nephrology, news release, Aug. 6, 2008
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