Laboratory for Molecular Diagnostics
Center for Nephrology and Metabolic Disorders
Moldiag Diseases Genes Support Contact

Mesangioproliferative glomerulonephritis

The most important mesangioproliferative glomerulonephritis is IgA nephropathy. Therefore in many textbooks it is considered as one and the same disease. However, the fact that mesangioproloferative glomerulonephritis can occur with other diseases such as lupus nephritis and the recently revealed genetic heterogeneity suggest different pathogentic mechanisms. Mesangioproliferative glomerulonephritis is a histomorphological diagnosis characterized by mesangial accumulation of cells and IgA deposits. Clinical picture is dominated by hematuria which is often accompanied by proteinuria and decline of renal function.

Classification

Morphological

Although most renal biopsies show IgA deposits, a small group of non-IgA mesangioproliferative glomerulonephritis can be distinguished.[Error: Macro 'ref' doesn't exist]

Pathogenetical

Primary and secodary forms can be distinguished. The latter includes diseases such as lupus nephropathy.

Genetical

Genetic factors can be grouped into risk factors and those that cause diseases that can be accompanied by mesangioproliferative glomerulonephritis. For instance, the deletion of the CFRH1 und CFRH3 genes is a well characterized risk factor, and diseases associated with mesangioproliferative glomerulonephritis include Wiskott–Aldrich syndrome, complement component C1q deficiency and Schimke Immunoosseous dysplasia.

Systematic

Glomerulonephritis
C3 glomerulopathy
CFHR5 Nephropathy
Goodpasture syndrome
Lupus erythematosus nephritis
Membranoproliferative glomerulonephritis (MPGN)
Membranous nephropathy
Mesangioproliferative glomerulonephritis
CXCR1
Complement component C1q deficiency
C1QA
C1QB
C1QC
IgA nephropathy
CFHR1
CFHR3
CFHR5
IgA nephropathy type 1
IgA nephropathy type 2
IgA nephropathy type 3
SPRY2
Schimke Immunoosseous dysplasia
SMARCAL1
Wiskott–Aldrich syndrome
WAS

References:

1.

Tolkoff-Rubin NE et al. (1978) IGA nephropathy in HLA-identical siblings.

external link
2.

None (1980) Splenectomy in the Wiskott-Aldrich syndrome.

external link
3.

Lum LG et al. (1980) Splenectomy in the management of the thrombocytopenia of the Wiskott-Aldrich syndrome.

external link
4.

Remold-O'Donnell E et al. (1984) Characterization of a human lymphocyte surface sialoglycoprotein that is defective in Wiskott-Aldrich syndrome.

external link
5.

Wyatt RJ et al. (2013) IgA nephropathy.

external link
6.

Gharavi AG et al. (2011) Genome-wide association study identifies susceptibility loci for IgA nephropathy.

external link
7.

Paterson AD et al. (2007) Genome-wide linkage scan of a large family with IgA nephropathy localizes a novel susceptibility locus to chromosome 2q36.

external link
8.

Obara W et al. (2003) Association of single-nucleotide polymorphisms in the polymeric immunoglobulin receptor gene with immunoglobulin A nephropathy (IgAN) in Japanese patients.

external link
9.

Tsuge T et al. (2001) Polymorphism in promoter region of Fcalpha receptor gene in patients with IgA nephropathy.

external link
10.

Shimokawa T et al. (2000) Identification and characterization of the promoter for the gene encoding the human myeloid IgA Fc receptor (FcalphaR, CD89).

external link
11.

Tomana M et al. (1997) Galactose-deficient IgA1 in sera of IgA nephropathy patients is present in complexes with IgG.

external link
12.

Katz A et al. (1980) Family study in IgA nephritis: the possible role of HLA antigens.

external link
13.

Holmberg L et al. (1983) A prenatal study of fetal platelet count and size with application to fetus at risk for Wiskott-Aldrich syndrome.

external link
14.

Brettle R et al. (1978) Mesangial IgA glomerulonephritis and HLA antigens.

external link
15.

Berthoux FC et al. (1978) HLA-Bw35 and mesangial IgA glomerulonephritis.

external link
16.

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.

external link
17.

Croker BP et al. (1983) IgA nephropathy. Correlation of clinical and histologic features.

external link
18.

McCoy RC et al. (1974) IgA nephropathy.

external link
19.

None (1969) IgA glomerular deposits in renal disease.

external link
20.

Jennette JC et al. (1985) Low incidence of IgA nephropathy in blacks.

external link
21.

Julian BA et al. (1985) Familial IgA nephropathy. Evidence of an inherited mechanism of disease.

external link
22.

Coppo R et al. (1986) Dietary gluten and primary IgA nephropathy.

external link
23.

Asamoah A et al. (1987) A major gene model for the familial aggregation of plasma IgA concentration.

external link
24.

Yamada M et al. (2000) Determination of carrier status for the Wiskott-Aldrich syndrome by flow cytometric analysis of Wiskott-Aldrich syndrome protein expression in peripheral blood mononuclear cells.

external link
25.

Cheungpasitporn W et al. (2011) Henoch-Schönlein purpura in an older man presenting as rectal bleeding and IgA mesangioproliferative glomerulonephritis: a case report.

external link
26.

Rathore SS et al. (2015) Mesangioproliferative glomerulonephritis in a patient with Kimura's disease presenting as Nephrotic syndrome.

external link
27.

Raghavan R et al. (2014) Takayasu arteritis: Association with mesangioproliferative glomerulonephritis in a 9-year-old child.

external link
28.

Axelsen M et al. (2014) Mesangioproliferative glomerulonephritis: a 30-year prognosis study.

external link
29.

Waikhom R et al. (2012) Non-IgA mesangioproliferative glomerulonephritis: a benign entity?

external link
30.

Boztug K et al. (2010) Stem-cell gene therapy for the Wiskott-Aldrich syndrome.

external link
31.

Puck JM et al. (2006) Lessons from the Wiskott-Aldrich syndrome.

external link
32.

VAN DEN BOSCH J et al. (1964) [THE ALDRICH SYNDROME; A CLINICAL AND GENETIC STUDY OF SEVERAL DUTCH FAMILIES].

external link
33.

GELZER J et al. (1961) [Wiskott-Aldrich syndrome].

external link
34.

None (1959) Methodology in human genetics.

external link
35.

Julian BA et al. (1988) IgA nephropathy, the most common glomerulonephritis worldwide. A neglected disease in the United States?

external link
36.

Yamada M et al. (1999) Flow cytometric analysis of Wiskott-Aldrich syndrome (WAS) protein in lymphocytes from WAS patients and their familial carriers.

external link
37.

Giliani S et al. (1999) Prenatal molecular diagnosis of Wiskott-Aldrich syndrome by direct mutation analysis.

external link
38.

Notarangelo LD et al. (1993) Application of molecular analysis to genetic counseling in the Wiskott-Aldrich syndrome (WAS).

external link
39.

Knox-Macaulay HH et al. (1993) X linked recessive thrombocytopenia.

external link
40.

Sullivan KE et al. (1994) A multiinstitutional survey of the Wiskott-Aldrich syndrome.

external link
41.

Prchal JT et al. (1980) Wiskott-Aldrich syndrome: cellular impairments and their implication for carrier detection.

external link
42.

Spitler LE et al. (1980) Nephropathy in the Wiskott-Aldrich syndrome.

external link
43.

Perry GS et al. (1980) The Wiskott-Aldrich syndrome in the United States and Canada (1892-1979).

external link
44.

Kapoor N et al. (1981) Reconstitution of normal megakaryocytopoiesis and immunologic functions in Wiskott-Aldrich syndrome by marrow transplantation following myeloablation and immunosuppression with busulfan and cyclophosphamide.

external link
45.

Hutter JJ et al. (1981) Results of a thymic epithelial transplant in a child with Wiskott-Aldrich syndrome and central nervous system lymphoma.

external link
46.

Parolini O et al. (1998) X-linked Wiskott-Aldrich syndrome in a girl.

external link
47.

ALDRICH RA et al. (1954) Pedigree demonstrating a sex-linked recessive condition characterized by draining ears, eczematoid dermatitis and bloody diarrhea.

external link
48.

Wada T et al. (2003) Second-site mutation in the Wiskott-Aldrich syndrome (WAS) protein gene causes somatic mosaicism in two WAS siblings.

external link
49.

Sasahara Y et al. (2002) Mechanism of recruitment of WASP to the immunological synapse and of its activation following TCR ligation.

external link
50.

Lutskiy MI et al. (2002) Wiskott-Aldrich syndrome in a female.

external link
51.

Wada T et al. (2001) Somatic mosaicism in Wiskott--Aldrich syndrome suggests in vivo reversion by a DNA slippage mechanism.

external link
52.

Devriendt K et al. (2001) Constitutively activating mutation in WASP causes X-linked severe congenital neutropenia.

external link
53.

Thompson LJ et al. () Unique and recurrent WAS gene mutations in Wiskott-Aldrich syndrome and X-linked thrombocytopenia.

external link
54.

Lemahieu V et al. (1999) Novel mutations in the Wiskott-Aldrich syndrome protein gene and their effects on transcriptional, translational, and clinical phenotypes.

external link
55.

Waisfisz Q et al. (1999) Spontaneous functional correction of homozygous fanconi anaemia alleles reveals novel mechanistic basis for reverse mosaicism.

external link
56.

Puck JM et al. (1998) X inactivation in females with X-linked disease.

external link
57.

Wada T et al. (2004) Multiple patients with revertant mosaicism in a single Wiskott-Aldrich syndrome family.

external link
58.

Greer WL et al. (1996) Identification of WASP mutations, mutation hotspots and genotype-phenotype disparities in 24 patients with the Wiskott-Aldrich syndrome.

external link
59.

Schindelhauer D et al. (1996) Wiskott-Aldrich syndrome: no strict genotype-phenotype correlations but clustering of missense mutations in the amino-terminal part of the WASP gene product.

external link
60.

Derry JM et al. (1995) The mouse homolog of the Wiskott-Aldrich syndrome protein (WASP) gene is highly conserved and maps near the scurfy (sf) mutation on the X chromosome.

external link
61.

Kolluri R et al. (1996) Direct interaction of the Wiskott-Aldrich syndrome protein with the GTPase Cdc42.

external link
62.

Symons M et al. (1996) Wiskott-Aldrich syndrome protein, a novel effector for the GTPase CDC42Hs, is implicated in actin polymerization.

external link
63.

Derry JM et al. (1994) Isolation of a novel gene mutated in Wiskott-Aldrich syndrome.

external link
64.

Villa A et al. (1995) X-linked thrombocytopenia and Wiskott-Aldrich syndrome are allelic diseases with mutations in the WASP gene.

external link
65.

Kwan SP et al. (1995) Identification of mutations in the Wiskott-Aldrich syndrome gene and characterization of a polymorphic dinucleotide repeat at DXS6940, adjacent to the disease gene.

external link
66.

Wengler G et al. (1995) Nonrandom inactivation of the X chromosome in early lineage hematopoietic cells in carriers of Wiskott-Aldrich syndrome.

external link
67.

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.

external link
68.

Hiki Y et al. (2001) Mass spectrometry proves under-O-glycosylation of glomerular IgA1 in IgA nephropathy.

external link
69.

None (1987) The commonest glomerulonephritis in the world: IgA nephropathy.

external link
70.

None (1989) Familial cases of Berger's disease and anaphylactoid purpura: more frequent than previously thought.

external link
71.

Suzuki H et al. (2008) IgA1-secreting cell lines from patients with IgA nephropathy produce aberrantly glycosylated IgA1.

external link
72.

Bisceglia L et al. (2006) Genetic heterogeneity in Italian families with IgA nephropathy: suggestive linkage for two novel IgA nephropathy loci.

external link
73.

Wang J et al. (2004) Dysregulated LIGHT expression on T cells mediates intestinal inflammation and contributes to IgA nephropathy.

external link
74.

Song J et al. (2003) Gender specific association of aldosterone synthase gene polymorphism with renal survival in patients with IgA nephropathy.

external link
75.

Yoon HJ et al. (2003) Association of the CD14 gene -159C polymorphism with progression of IgA nephropathy.

external link
76.

Donadio JV et al. (2002) IgA nephropathy.

external link
77.

Takei T et al. (2002) Association between single-nucleotide polymorphisms in selectin genes and immunoglobulin A nephropathy.

external link
78.

Allen AC et al. (2001) Mesangial IgA1 in IgA nephropathy exhibits aberrant O-glycosylation: observations in three patients.

external link
79.

Pei Y et al. (1997) Association of angiotensinogen gene T235 variant with progression of immunoglobin A nephropathy in Caucasian patients.

external link
80.

Gharavi AG et al. (2000) IgA nephropathy, the most common cause of glomerulonephritis, is linked to 6q22-23.

external link
81.

Hsu SI et al. (2000) Evidence for genetic factors in the development and progression of IgA nephropathy.

external link
82.

Zheng F et al. (1999) Uteroglobin is essential in preventing immunoglobulin A nephropathy in mice.

external link
83.

Scolari F et al. (1999) Familial clustering of IgA nephropathy: further evidence in an Italian population.

external link
84.

Song J et al. (2003) Peroxisome proliferator-activated receptor gamma C161T polymorphisms and survival of Japanese patients with immunoglobulin A nephropathy.

external link
85.

Milillo A et al. (2015) A SPRY2 mutation leading to MAPK/ERK pathway inhibition is associated with an autosomal dominant form of IgA nephropathy.

external link
86.

Boztug K et al. (2008) Multiple independent second-site mutations in two siblings with somatic mosaicism for Wiskott-Aldrich syndrome.

external link
87.

Dobbs AK et al. (2007) A possible bichromatid mutation in a male gamete giving rise to a female mosaic for two different mutations in the X-linked gene WAS.

external link
88.

Binder V et al. (2006) The genotype of the original Wiskott phenotype.

external link
89.

Du W et al. (2006) A second-site mutation in the initiation codon of WAS (WASP) results in expansion of subsets of lymphocytes in an Wiskott-Aldrich syndrome patient.

external link
Update: Aug. 14, 2020
Copyright © 2005-2024 by Center for Nephrology and Metabolic Disorders, Dr. Mato Nagel, MD
Albert-Schweitzer-Ring 32, D-02943 Weißwasser, Germany, Tel.: +49-3576-287922, Fax: +49-3576-287944
Sitemap | Webmail | Disclaimer | Privacy Issues | Website Credits