IgA Nephropathy (IgAN)

IgA Nephropathy, clinically termed Berger's disease, is an autoimmune disorder marked by the presence of IgA antibodies in the glomeruli of the kidneys. This disease, first identified in 1968 by Jean Berger, has since been recognized as a leading cause of glomerulonephritis globally. Its prevalence varies geographically, being more common in East Asia and less so in North America and Europe.

The pathogenesis of IgA Nephropathy involves the abnormal accumulation of IgA antibodies in the kidneys, leading to inflammation and, over time, potential kidney damage. The disease progresses at varying rates among individuals, with some experiencing a rapid decline in kidney function while others may have a more indolent course.

Symptoms of IgA Nephropathy often include hematuria (blood in urine), proteinuria (protein in urine), and hypertension. However, many patients remain asymptomatic in the early stages, making early diagnosis challenging. Long-term implications can be severe, with a significant number of patients progressing to end-stage renal disease (ESRD) within 20 to 30 years of diagnosis.

The diagnosis of IgA Nephropathy typically involves a combination of laboratory tests, including blood and urine analysis, and often a renal biopsy to confirm the presence of IgA deposits in the kidney tissues. Genetic, environmental, and immunological factors are believed to contribute to the development and progression of the disease.

Treatment strategies for IgA Nephropathy primarily focus on controlling symptoms and preventing further kidney damage. This includes managing blood pressure, reducing proteinuria, and using medications such as corticosteroids, immunosuppressants, or fish oil. The effectiveness of these treatments varies, highlighting the need for continued research and development of more targeted therapies.