IgA Nephropathy
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Basics
Description
- Most common form of glomerulonephritis in the world
- Renal parenchymal damage and dysfunction defined by deposition of IgA in glomerular mesangium
- Significant contributor to the incidence of end-stage renal disease (ESRD) in parts of Asia
Epidemiology
Incidence
In patients who undergo renal biopsy, the following incidence was reported: 30–40% in Asia, 15–20% in Europe, and 5–10% in North America
Prevalence
- Highest prevalence in Pacific Rim, particularly Japan and Korea
- More common in Asians, whites, and American Indians versus blacks in the United States and Africa
Etiology and Pathophysiology
Genetics
- Familial forms of IgA nephropathy (IgAN) exist with no specific gene identified.
- IgA1 molecules deposit within the mesangium leading to an inflammatory reaction with eventual fibrosis and scarring of the nephron.
Risk Factors
- Liver disease: Impaired removal of IgA by Kupffer cells in the liver predisposes individuals to IgA deposition in the kidney.
- Celiac disease: Ingestion of gliadin results in the formation of IgA antigliadin antibodies and deposition of immune complexes in the kidney.
Commonly Associated Conditions
- Henoch-Schönlein purpura
- Hepatic failure
- Celiac disease
- Rheumatoid arthritis
- Ankylosing spondylitis
- Reiter syndrome
- HIV
- CMV
-- To view the remaining sections of this topic, please log in or purchase a subscription --
Basics
Description
- Most common form of glomerulonephritis in the world
- Renal parenchymal damage and dysfunction defined by deposition of IgA in glomerular mesangium
- Significant contributor to the incidence of end-stage renal disease (ESRD) in parts of Asia
Epidemiology
Incidence
In patients who undergo renal biopsy, the following incidence was reported: 30–40% in Asia, 15–20% in Europe, and 5–10% in North America
Prevalence
- Highest prevalence in Pacific Rim, particularly Japan and Korea
- More common in Asians, whites, and American Indians versus blacks in the United States and Africa
Etiology and Pathophysiology
Genetics
- Familial forms of IgA nephropathy (IgAN) exist with no specific gene identified.
- IgA1 molecules deposit within the mesangium leading to an inflammatory reaction with eventual fibrosis and scarring of the nephron.
Risk Factors
- Liver disease: Impaired removal of IgA by Kupffer cells in the liver predisposes individuals to IgA deposition in the kidney.
- Celiac disease: Ingestion of gliadin results in the formation of IgA antigliadin antibodies and deposition of immune complexes in the kidney.
Commonly Associated Conditions
- Henoch-Schönlein purpura
- Hepatic failure
- Celiac disease
- Rheumatoid arthritis
- Ankylosing spondylitis
- Reiter syndrome
- HIV
- CMV
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