IgA nephropathy is a chronic kidney disease that usually first appears during adolescence and young adulthood and often progresses to kidney failure. It usually follows a viral infection of the upper respiratory or gastrointestinal tracts. The major symptom is the passing of blood in the urine (hematuria). There may be associated pain in the loin area.
The first recognizable symptom of IgA nephropathy is bloody urine (hematuria) caused by inflammation of the kidney (acute nephritis or glomerulonephritis). There is often a mild loss of protein in the urine (proteinuria) with slowly progressive changes in the kidney. Pain in the loins may occur, but it is unusual for people with this condition to show signs of high blood pressure (hypertension) or swelling (edema) during the initial phase of the disease.
IgA nephropathy usually occurs following flu-like (viral) infections of the upper respiratory tract or the gastrointestinal tract. This suggests it may be caused by a postinfectious process. There are some theories that the condition is an autoimmune disease because of the increase in the immunoglobulin IgA factor, but the mechanisms leading to glomerular immune deposit formation is unclear. Autoimmune disorders are caused when the body’s natural defenses against “foreign” or invading organisms (e.g., antibodies) begin to attack healthy tissue for unknown reasons.
IgA nephropathy affects males two or three times more often than females. It usually occurs in adolescents or young adults between the ages of fifteen and thirty-five. It is believed to affect as many as 130,000 people annually in the United States, and is one of the leading causes of acute nephritis in young people in the United States, Europe and Japan. IgA nephropathy occurs significantly more often in American Indians than any other ethnic group tested. It is more prevalent in Americans of European descent than in Americans of African descent. A study conducted in Finland showed an occurrence of approximately 94 cases detected annually per 100,000 young males tested upon induction into the military.
No specific treatment for IgA nephropathy has been shown to be effective to all patients. Some patients have responded to oral steroid therapy especially in the early stages of the disease. Patients who have been treated with the corticosteroid drug, cyclophosamide, have experienced long- term remission of symptoms even after therapy was withdrawn. The disease may progress slowly for several decades and can lead to other kidney (renal) diseases such as renal insufficiency. Kidney transplantation has been successful in many persons, although some patients have an immunologic recurrence of disease in the new kidney.
Information on current clinical trials is posted on the Internet at www.clinicaltrials.gov. All studies receiving U.S. government funding, and some supported by private industry, are posted on this government web site.
For information about clinical trials being conducted at the NIH Clinical Center in Bethesda, MD, contact the NIH Patient Recruitment Office:
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For information about clinical trials sponsored by private sources, contact:
On Dec 3rd of 2007 BioMarin Pharmaceuticals and IGAN Biosciences announced a collaboration to initiate a program to develop an IgA protease for treating IgA Nephropathy. IgA protease is shown to cleave the IgA complex which can casue the nephropathy.
BioMarin has executed a research and option agreement with IGAN Bioseciences for intellectual property covering IgA protease for treating IgA nephropathy.
For more information on both companies and further details please visit their website
IGAN Biosciences- www.iganbio.com
BioMarin Pharmceutical Inc-www.BMRN.com
CuraGen Corporation of New Haven, CT, announced on November 11, 2004, that its drug, CR002, a human monoclonal antibody, was granted FDA orphan drug status as a potential treatment to slow the progression of IgA nephropathy and delay kidney failure in patients affected by the disease. The drug is in a Phase I trial. For information, contact the company at:
555 Long Wharf Drive
New Haven, CT 06511
Tel.: (888) GENOMICS
Fax: (203) 401-3331
Omega-3 (n-3) polyunsaturated fatty acids (Omacor) received orphan product designation for treatment of IgA nephropathy in May, 2000. The drug is produced by Pronova Biocare, PO Box 420, 1327 Lysaker, Norway.
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FROM THE INTERNET
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