Disease relevance of Glomerulonephritis, Membranoproliferative

• One child with heterozygous C3 deficiency was found to have membranoproliferative glomerulonephritis; proteinuria and/or microscopical haematuria was present in all three homozygous C3-deficient children [1].
• Nephritic factor of the alternative complement pathway (C3NeF) is an IgG autoantibody which binds to and stabilizes the C3 convertase (C3bBb) enzyme, and which has been detected mainly in sera from patients with membranoproliferative glomerulonephritis (MPGN) and partial lipodystrophy [2].
• By 6 months of age, ABCA1-/- animals develop membranoproliferative glomerulonephritis due to deposition of immunocomplexes followed by cardiomegaly with ventricular dilation and hypertrophy, ultimately succumbing to congestive heart failure [3].
• In contrast, no remarkable TbetaRII expression was noted in mesangial proliferative lesions in IgA nephropathy, lupus nephritis, and membranoproliferative glomerulonephritis [4].
• The proliferation of MC is a prominent feature of glomerular disease including IgA nephropathy, membranoproliferative glomerulonephritis, lupus nephritis, and diabetic nephropathy [5].

High impact information on Glomerulonephritis, Membranoproliferative

• Here we show that mice deficient in factor H (Cfh(-/-) mice) develop MPGN spontaneously and are hypersensitive to developing renal injury caused by immune complexes [6].
• Uncontrolled C3 activation causes membranoproliferative glomerulonephritis in mice deficient in complement factor H [6].
• Renal biopsy in all patients revealed membranoproliferative glomerulonephritis, characterized by the deposition of IgG, IgM, and C3 in glomeruli [7].
• Forty patients with Type I membranoproliferative glomerulonephritis were treated for one year with dipyridamole, 225 mg per day, and aspirin, 975 mg per day, in a prospective, randomized, double-blind, placebo-controlled study [8].
• The study was designed to examine the metabolism of properdin in normal subjects and to look for an abnormality in five patients with systemic lupus erythematosus with renal involvement and in six patients with membranoproliferative glomerulonephritis or dense deposit disease (MPGN) [9].

Chemical compound and disease context of Glomerulonephritis, Membranoproliferative

• Lectin binding in membranoproliferative glomerulonephritis. Evidence for N-acetylglucosamine in dense intramembranous deposits [10].
• The one recurrence of type I membranoproliferative glomerulonephritis was associated with depressed C3, Clq, C4 and factor B but without C3NeF activity [11].
• A prospective trial of warfarin and dipyridamole was performed in patients with membranoproliferative glomerulonephritis [12].
• A patient with membranoproliferative glomerulonephritis and renal dysfunction caused by Schistosoma mansoni was treated with oxamniquine [13].
• The effect of prednisone in a high-dose, alternate-day regimen on the natural history of idiopathic membranoproliferative glomerulonephritis [14].

Biological context of Glomerulonephritis, Membranoproliferative

• Significant impact on graft survival was seen with recurrent and de novo FSGS, membranoproliferative glomerulonephritis, and HUS/TTP [15].
• This study investigates the influence of aspirin plus dipyridamole on proteinuria and renal function in nephrotic MPGN patients with moderately reduced glomerular filtration rate [16].
• The most common extended haplotype [HLA-B8, DR3, SC01], when it carries GLO2, is increased in type I diabetes mellitus and probably a number of other diseases, including gluten-sensitive enteropathy and membranoproliferative glomerulonephritis [17].
• Although it is unclear how MPGN occurred in this XLA patient, we suggest that residual humoral immunity in the patient could be associated with the development of MPGN [18].
• Fifty children with idiopathic membranoproliferative glomerulonephritis (MPGN), aged 2-14 years at apparent onset, were monitored for the presence of C3 nephritic factor (C3 NeF) and signs of complement activation in serum [19].

Anatomical context of Glomerulonephritis, Membranoproliferative

• The combination of aspirin and dipyridamole prevents both early and late occlusion of saphenous vein aortocoronary bypass grafts and protects renal function in patients with membranoproliferative glomerulonephritis [20].
• Monocyte recruitment in cryoglobulinemic membranoproliferative glomerulonephritis: a pathogenetic role for monocyte chemotactic peptide-1 [21].
• On the contrary, no significant alteration was found in the peripheral T cell distribution of patients with membranoproliferative GN (MPGN) and lipoid nephrosis associated with minimal-change GN (MCGN) [22].
• Significant glomerular and vascular deposition of platelet antigen (or antigens) was observed along the endothelium or as vascular plugs in kidney tissue from patients with hemolytic uremic syndrome, membranoproliferative glomerulonephritis (types I and II), diabetic nephropathy, hypertensive renal disease, scleroderma, and other diseases [23].
• Low PAg was the consequence of incubation of normal phagocytes with the earliest available sera from all 22 P-SGN patients, 28 of 37 SLE-GN patients, 19 of 25 patients with MPGN type I, all 10 with types II and III, and all 5 with nephritis associated with chronic bacteremia [24].

Gene context of Glomerulonephritis, Membranoproliferative

• In microdissected glomeruli of normal and non-HCV membranoproliferative glomerulonephritis biopsies, TLR3 mRNA expression was low [25].
• Scattered PTX3-positive cells were also detected in glomeruli of type I membranoproliferative glomerulonephritis [26].
• Fibronectin is a multidomain glycoprotein which accumulates in mesangial proliferative glomerulonephritis (MPGN) [27].
• Recent evidence has implicated transforming growth factor beta (TGF-beta) in the pathogenesis of experimental MPGN [27].
• (4) Conversely, cytokine measurements showed high serum IL-2 and IL-2R values in the LN and MPGN groups, and serum IL-4 values were high in the MGN group [28].

Analytical, diagnostic and therapeutic context of Glomerulonephritis, Membranoproliferative

• Massive glomerular deposits of C3 and the terminal C5b-9 complement complex (TCC), but no immune complex deposits were detected by immunofluorescence in porcine membranoproliferative glomerulonephritis type II [29].
• Therefore, a retrospective comparative analysis of 75 patients with MPGN II contained in the North American Pediatric Renal Transplant Cooperative Study transplantation database was performed [30].
• Immunizations were started in 6- to 8-wk-old mice, which was before the development of spontaneous membranoproliferative glomerulonephritis in some Cfh(-/-) animals [31].
• However, in serum from 13 MPGN patients containing large amounts of spClq-binding material, sucrose density ultracentrifugation and sieve chromatography showed spClq-binding protein to sediment at 7S or cofractionate with IgG [32].
• Laser capture microdissection (LCM) was performed to isolate and collect glomeruli and tubules from 20 consecutive chronically HCV-infected patients, namely 6 with membranoproliferative glomerulonephritis, 4 with membranous glomerulonephritis, 7 with focal segmental glomerulosclerosis and 3 with IgA-nephropathy [33].

References