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IgA nephropathy is an autoimmune kidney disorder with symptoms ranging from transient episodes of bloody urine to renal failure.
Berger’s disease, which is also know as IgA nephropathy, is an autoimmune kidney disorder first described by Berger and Hinglais in 1968. A form of mesangial proliferative nephritis (inflammation of the kidney’s function units), Berger’s disease causes inflammation in the glomeruli, resulting in a condition of chronic glomerulonephritis. In addition, immunoglobulin A (IgA) and immune complex deposits lodge into kidney tissue, interfering with kidney function. IgA nephropathy is the most common cause of glomerulonephritis in the world. Symptoms and SignsBerger’s disease causes blood in the urine, ranging from periodic presentations of blood (hematuria) and protein (proteinuria) in the urine observed microscopically to episodes of dark, brown, rust-colored, or bloody urine. The disease course is highly variable, ranging from occasional episodes of microscopic hematuria to conditions of rapidly progressive glomerulonephritis (RPGN). Symptoms may occur transiently and slowly progress to acute nephritic syndrome or nephritic syndrome (groups of symptoms associated with decreased kidney function, for instance elevated blood levels of blood urea nitrogen (BUN) and creatinine and hypertension) or appear suddenly and progress rapidly. About 25 percent of people with Berger’s disease develop end-stage kidney failure within about 25 years (IgA Nephropathy, Medline Plus Medical Encyclopedia, Sept 13, 2005). Who is Affected?IgA nephropathy can occur in both males and females of all ages although the disease primarily targets in males in their teens through their late 30s and is rarely seen in children younger than 10 years old. Berger’s disease is more common in whites and Asians and is rare in Blacks, both in the United States and in Africa. Berger’s disease is frequently seen in American Indians of the Zuni and Navajo tribes. Symptoms may begin soon after a respiratory infection. People with a family history of IgA nephropathy or Henoch-Schonlein purpura are at increased risk for developing Berger’s disease. DiagnosisAn examination of the urine (urinalysis) may show red blood cells, red blood cell casts, protein, and elevated fats. Urine immunoelectropheresis tests show antibodies to IgA. Kidney biopsy shows deposits of IgA, which are diagnostic for Berger’s disease, and deposits of complement. TreatmentTreatment is used in an effort to prevent disease progression and delay chronic renal failure. Antihypertensive (high blood pressure) medications, including diuretics, are used to reduce blood pressure and edema (fluid retention). Salt restriction is recommended to prevent swelling. ACE inhibitors are especially important for reducing disease prevention. Corticosteroids and other immunosuppressive drugs may also be used to reduce inflammation. Associated DisordersIgA nephropathy does not cause systemic disease (affecting multiple organs) although many systemic diseases, particularly Henoch-Schonlein purpura) are sporadically associated with IgA deposits in the kidneys. Other autoimmune systemic diseases in which IgA deposits are regularly observed include:
Other diseases in which episodes of IgA deposits in the urine may occur include:
Resources:IgA Nephropathy Support Network Mona Brake, IgA Nephropathy, eMedicine from WebMD, April 9, 2007, accessed June 11, 2007.
The copyright of the article Bloody Urine in Autoimmune Disease is owned by Elaine Moore. Permission to republish Bloody Urine in print or online must be granted by the author in writing.
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