Klinik: 

Definition: Die IgA-Nephropathie ist die häufigste Form der Glomerulonephritis. Immunhistologisch ist es eine mesangioproliferative Glomerulonephritis mit verstärkter IgA-Ablagerung. Meist ist auch im Serum ein erhöhter IgA-Spiegel nachweisbar.

Pathogenese: Der Verlauf der IgA-Nephropathie ist individuell sehr unterschiedlich. Während einige Patienten über Jahre stabil bleiben, gelangen andere relativ rasch in das Stadium der terminalen Niereninsuffizienz. Die Ursachen für diese individuellen Unterschiede sind noch bei weitem nicht aufgeklärt. Neben der effektiven Blutdrucksenkung mit einer Blockade des Renin-Angiotensin-Systems und diätetischen Maßnahmen (Polyen-Fettsäuren sog. Fischöl) scheinen auch genetische Faktoren eine Rolle zu spielen.

Literatur: 

Segerer S et al. (1999) Expression of the C-C chemokine receptor 5 in human kidney diseases.
Allen AC et al. (2001) Mesangial IgA1 in IgA nephropathy exhibits aberrant O-glycosylation: observations in three patients.
Asamoah A et al. (1987) A major gene model for the familial aggregation of plasma IgA concentration.
Bene MC et al. (1983) Immunoglobulin A nephropathy. Quantitative immunohistomorphometry of the tonsillar plasma cells evidences an inversion of the immunoglobulin A versus immunoglobulin G secreting cell balance.
Berger J et al. (1969) IgA glomerular deposits in renal disease.
Berthoux FC et al. (1978) HLA-Bw35 and mesangial IgA glomerulonephritis.
Bisceglia L et al. (2006) Genetic heterogeneity in Italian families with IgA nephropathy: suggestive linkage for two novel IgA nephropathy loci.
Brettle R et al. (1978) Mesangial IgA glomerulonephritis and HLA antigens.
Coppo R et al. (1986) Dietary gluten and primary IgA nephropathy.
Croker BP et al. (1983) IgA nephropathy. Correlation of clinical and histologic features.
D'Amico G et al. (1987) The commonest glomerulonephritis in the world: IgA nephropathy.
Donadio JV et al. (2002) IgA nephropathy.
Gharavi AG et al. (2000) IgA nephropathy, the most common cause of glomerulonephritis, is linked to 6q22-23.
Hiki Y et al. (2001) Mass spectrometry proves under-O-glycosylation of glomerular IgA1 in IgA nephropathy.
Hsu SI et al. (2000) Evidence for genetic factors in the development and progression of IgA nephropathy.
Jennette JC et al. (1985) Low incidence of IgA nephropathy in blacks.
Julian BA et al. (1985) Familial IgA nephropathy. Evidence of an inherited mechanism of disease.
Julian BA et al. (1988) IgA nephropathy, the most common glomerulonephritis worldwide. A neglected disease in the United States?
Katz A et al. (1980) Family study in IgA nephritis: the possible role of HLA antigens.
Levy M et al. (1989) Familial cases of Berger's disease and anaphylactoid purpura: more frequent than previously thought.
McCoy RC et al. (1974) IgA nephropathy.
Pei Y et al. (1997) Association of angiotensinogen gene T235 variant with progression of immunoglobin A nephropathy in Caucasian patients.
Sabatier JC et al. (1979) Mesangial IgA glomerulonephritis in HLA-identical brothers.
Scolari F et al. (1999) Familial clustering of IgA nephropathy: further evidence in an Italian population.
Song J et al. (2003) Gender specific association of aldosterone synthase gene polymorphism with renal survival in patients with IgA nephropathy.
Suzuki H et al. (2008) IgA1-secreting cell lines from patients with IgA nephropathy produce aberrantly glycosylated IgA1.
Takei T et al. (2002) Association between single-nucleotide polymorphisms in selectin genes and immunoglobulin A nephropathy.
Tolkoff-Rubin NE et al. (1978) IGA nephropathy in HLA-identical siblings.
Tomana M et al. (1997) Galactose-deficient IgA1 in sera of IgA nephropathy patients is present in complexes with IgG.
Wang J et al. (2004) Dysregulated LIGHT expression on T cells mediates intestinal inflammation and contributes to IgA nephropathy.
Yoon HJ et al. (2003) Association of the CD14 gene -159C polymorphism with progression of IgA nephropathy.
Yoshida H et al. (1995) Role of the deletion of polymorphism of the angiotensin converting enzyme gene in the progression and therapeutic responsiveness of IgA nephropathy.
Zheng F et al. (1999) Uteroglobin is essential in preventing immunoglobulin A nephropathy in mice.