Immunoglobulin A Nephropathy

(IgA nephropathy, Berger’s disease)

IgA nephropathy (IgAN) is a deposition of IgA immune complexes in the glomeruli. It manifests itself as a slowly progressive hematuria, proteinuria and renal failure often. The diagnosis is based on the findings of urine and renal biopsy. The prognosis is generally good. As treatment options are ACE inhibitors, angiotensin II receptor antagonists, corticosteroids, immunosuppressants and polyunsaturated omega-3 fatty acid into consideration.

IgA nephropathy (IgAN) is a nephritic syndrome, a form of chronic glomerulonephritis (GN), which is characterized by the deposition of IgA-immune complexes in the glomeruli. It is the most common form of the GN and occurs in all age groups, with the disease peaks between teens and the third decade of life is. It occurs in all age groups, where the disease peaks between teens and the third decade of life is. The IgAN occurs in men two to six times more frequently than women and in Caucasians and Asians more common than dark-skinned people. It is estimated that the prevalence of “IgA kidney deposits” in the US 5%, in southern Europe and Australia is 10-20% and in Asia from 30 to 40%. However, some people do not develop clinical disease with IgA deposits.

IgA nephropathy (IgAN) is a deposition of IgA immune complexes in the glomeruli. It manifests itself as a slowly progressive hematuria, proteinuria and renal failure often. The diagnosis is based on the findings of urine and renal biopsy. The prognosis is generally good. As treatment options are ACE inhibitors, angiotensin II receptor antagonists, corticosteroids, immunosuppressants and polyunsaturated omega-3 fatty acid into consideration. IgA nephropathy (IgAN) is a nephritic syndrome, a form of chronic glomerulonephritis (GN), which is characterized by the deposition of IgA-immune complexes in the glomeruli. It is the most common form of the GN and occurs in all age groups, with the disease peaks between teens and the third decade of life is. It occurs in all age groups, where the disease peaks between teens and the third decade of life is. The IgAN occurs in men two to six times more frequently than women and in Caucasians and Asians more common than dark-skinned people. It is estimated that the prevalence of “IgA kidney deposits” in the US 5%, in southern Europe and Australia is 10-20% and in Asia from 30 to 40%. However, some people do not develop clinical disease with IgA deposits. Cause is unknown, but evidence suggests that there are several mechanisms, including Increased IgA1 production defects IgA1 glycosylation, resulting in increased binding to the mesangial cells Decreased IgA1 clearance A defective mucosal immune system The overproduction of cytokines stimulating mesangial cell proliferation Familial clustering has also been observed, suggesting at least in some cases, to genetic factors. The renal function is initially normal, but it can develop symptomatic kidney disease. Some patients develop acute kidney injury or chronic kidney disease, severe hypertension or nephrotic syndrome. Symptoms and signs The most common manifestations are persistent or recurrent macroscopic hematuria or microscopic hematuria asymptomatic low proteinuria. Flank pain and low-grade fever may accompany acute episodes. Other symptoms usually are not prominent. A gross hematuria usually begins 1-2 days after a febrile mucosal disease (upper respiratory tract, sinuses, intestines) which masluxiert the acute post-infectious GN, unless begins earlier and hematuria occurs along with or shortly after the febrile attack. A rapidly progressive GN is the initial manifestation in <10% of patients. Diagnostic urinalysis Sometimes renal biopsy The diagnosis is suspected because of the following: gross hematuria, particularly within 2 days after a febrile mucosal disease or flank pain Coincidentally established findings on urinalysis Occasionally rapidly progressive GN If the manifestations of moderate or severe, the diagnosis is a biopsy confirmed. Urinalysis is a microscopic hematuria, usually with dysmorphic erythrocytes and erythrocytes occasionally cylinders. Nephrotic syndrome develops in ? 20% of cases. A slight proteinuria (<1 g / day) is typical and can occur without hematuria. The serum creatinine levels are usually normal. IgA nephropathy (IgA Mesangial deposition) Figure provided by Agnes Fogo, M.D., and the American Journal of Kidney Disease, Atlas of Renal Pathology (see www.ajkd.org). var model = {thumbnailUrl: '/-/media/manual/professional/images/iga_nephropathy_mesangial_iga_deposition_high_de.jpg?la=de&thn=0&mw=350' imageUrl: '/-/media/manual/professional/images/iga_nephropathy_mesangial_iga_deposition_high_de.jpg?la = en & thn = 0 ', title:' IgA nephropathy (IgA Mesangial deposition) 'description:' u003Ca id = "v38396886 " class = ""anchor "" u003e u003c / a u003e u003cdiv class = ""para "" u003e u003cp u003eImmunfluoreszenzfärbung with anti-IgA of granular mesangial IgA deposition ( u003cspan class = ""symbol "" u003e × u003c / span u003e200). u003c / p u003e u003c / div u003e 'credits' figure provided by Agnes Fogo

Health Life Media Team

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