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Glomerulonephritis Causes

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2121. Renoprotective effect of small doses of losartan and enalapril in patients with primary glomerulonephritis. Short-term observation. (PubMed)

-treated subjects. No changes in serum creatinine level, metabolic profile and sodium excretion were observed during therapy in studied groups.These results indicated that even very small doses of losartan and enalapril reduce proteinuria in patients with primary glomerulonephritis. Combination of these drugs could cause significantly greater antiproteinuric effect than either of the agents in monotherapy. It is likely that the treatment with losartan, compared to enalapril, is associated with less (...) Renoprotective effect of small doses of losartan and enalapril in patients with primary glomerulonephritis. Short-term observation. The renin-angiotensin system is thought to be involved in progression of chronic renal diseases of both diabetic and nondiabetic origin. It is confirmed that angiotensin-converting enzyme inhibitors reduce urinary protein excretion (UPE) and attenuate the development of renal injury. The angiotensin II receptor blockers are an alternative class of drugs inhibiting

2002 American journal of nephrology

2122. Membranoproliferative glomerulonephritis develops in a child with autologous stem cell transplant. (PubMed)

Membranoproliferative glomerulonephritis develops in a child with autologous stem cell transplant. Bone marrow transplant nephropathy is a known complication of bone marrow transplantation. Bone marrow transplantation can cause various rare kidney diseases such as membranous nephropathy and focal segmental glomerulosclerosis. Idiopathic membranoproliferative glomerulonephritis is rare in children. Here the authors report on a 5-year-old pediatric autologous stem cell recipient, in whom type I (...) membranoproliferative glomerulonephritis developed 111 days after bone marrow transplantation and presented with hematuria, hypertension, proteinuria, and renal failure.Copyright 2002 by the National Kidney Foundation, Inc.

2002 American Journal of Kidney Diseases

2123. Reversal of established rat crescentic glomerulonephritis by blockade of macrophage migration inhibitory factor (MIF): potential role of MIF in regulating glucocorticoid production. (PubMed)

with a significant reduction in leukocyte infiltration and activation and renal interleukin-1 (IL-1) production. Importantly, anti-MIF Ab treatment caused a significant increase in endogenous serum corticosterone levels, which correlated with the reversal of disease parameters. In conclusion, this study has demonstrated that blocking MIF activity can partially reverse established crescentic glomerulonephritis and suggests that MIF operates by both enhancing the cellular immune response and suppressing (...) Reversal of established rat crescentic glomerulonephritis by blockade of macrophage migration inhibitory factor (MIF): potential role of MIF in regulating glucocorticoid production. Macrophage migration inhibitory factor (MIF) is a potent pro-inflammatory cytokine that also counter-regulates glucocorticoid action. We investigated whether immunoneutralization of MIF could reverse established experimental crescentic glomerulonephritis and if this treatment could modulate endogenous glucocorticoid

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1998 Molecular Medicine

2124. Reduced nitric oxide synthase activity in rats with chronic renal disease due to glomerulonephritis (PubMed)

Reduced nitric oxide synthase activity in rats with chronic renal disease due to glomerulonephritis Animal studies with systemic nitric oxide synthase (NOS) inhibition and renal ablation, suggest that NO deficiency is both a cause and a consequence of chronic renal disease (CRD).This study examined a glomerulonephritis (GN) model of CRD to determine if NO is deficient. In addition to measuring indices of renal function (proteinuria, creatinine clearance, structural damage), indices of total

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2002 Kidney International

2125. Typhoid glomerulonephritis. (PubMed)

Typhoid glomerulonephritis. 15 patients with typhoid glomerulonephritis were studied and compared with a group of children with poststreptococcal nephritis. Useful criteria distinguishing the two diseases are given. The diseases may present in a similar manner and therefore it is important to remember typhoid as a cause of glomerulonephritis in endemic areas or in patients travelling from endemic areas.

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1980 Archives of Disease in Childhood

2126. Macrophage-induced glomerular fibrin deposition in experimental glomerulonephritis in the rabbit. (PubMed)

without macrophages. Thus macrophages appear to be directly responsible for glomerular fibrin deposition in antiglomerular basement membrane antibody-induced glomerulonephritis, and this appears to be due to their ability to express procoagulant activity rather than their propensity to cause glomerular injury. (...) Macrophage-induced glomerular fibrin deposition in experimental glomerulonephritis in the rabbit. Glomerular fibrin deposition is important in the pathogenesis of renal failure and crescent formation in glomerulonephritis. The mechanisms of glomerular fibrin deposition are unknown. The current studies explored the role of macrophages in this process. Methods were developed for measuring glomerular fibrin deposition and glomerular procoagulant activity in a passive model of the autologous phase

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1985 Journal of Clinical Investigation

2127. Haematuria in rheumatoid arthritis: an association with mesangial glomerulonephritis. (PubMed)

Haematuria in rheumatoid arthritis: an association with mesangial glomerulonephritis. Twenty-four patients with rheumatoid arthritis and isolated haematuria were investigated for the cause of their haematuria. In 3 patients local urological disorders were identified, including a pelvicaliceal carcinoma. Renal biopsies were performed on the remaining 21 patients, and the most common abnormality found was a mild mesangial glomerulonephritis (71%). Immunofluorescence and electron microscopy

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1984 Annals of the Rheumatic Diseases

2128. Dysgonic fermenter 2 infection resulting in chronic glomerulonephritis (PubMed)

Dysgonic fermenter 2 infection resulting in chronic glomerulonephritis Dysgonic fermenter 2 (DF-2) is a fastidious gram-negative pathogen that is capable of causing multiorgan disease in humans. In the case reported here infection resulted in subacute bacterial endocarditis, brain abscess and chronic type 1 membranoproliferative glomerulonephritis, a form of renal disease not previously reported in DF-2 infections. The literature is reviewed, and difficulties in diagnosis and treatment

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1985 Canadian Medical Association Journal

2129. Production of a novel class of polyreactive pathogenic autoantibodies in BXD2 mice causes glomerulonephritis and arthritis. (PubMed)

Production of a novel class of polyreactive pathogenic autoantibodies in BXD2 mice causes glomerulonephritis and arthritis. The BXD2 mouse strain spontaneously develops glomerulonephritis and erosive arthritis. The goal of this study was to identify the antigenic target proteins and epitopes and to unravel the mechanisms by which the related conditions arise in BXD2 mice.Individual hybridomas isolated from the spleen of a 10-month-old BXD2 mouse were injected intraperitoneally (...) , ATP5b, alpha-actin, and Hsp70 family proteins including Hspa5 and Hsp74. The antigenic epitopes of NT-modified enolase and Hspa5 exhibited sequence homology and cross-reactivity, suggesting that epitope spreading may occur through a molecular mimicry mechanism.The polyreactivity of autoantibodies that target a novel class of autoantigens may enable these autoantibodies to induce erosive arthritis or glomerulonephritis either by direct pathogenic mechanisms or indirectly via Fc or immune complex

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2006 Arthritis and Rheumatism

2130. Visual impairment caused by retinal abnormalities in mesangiocapillary (membranoproliferative) glomerulonephritis type II ("dense deposit disease"). (PubMed)

Visual impairment caused by retinal abnormalities in mesangiocapillary (membranoproliferative) glomerulonephritis type II ("dense deposit disease"). Patients with mesangiocapillary glomerulonephritis (MCGN) type II usually present by early adulthood with hematuria, proteinuria, and renal impairment, and these features often are accompanied by a partial lipodystrophy and an autoantibody for the alternative complement pathway convertase (C3NeF). The diagnosis of MCGN type II depends

2003 American Journal of Kidney Diseases

2131. Hypothesis: dysregulation of immunologic balance resulting from hygiene and socioeconomic factors may influence the epidemiology and cause of glomerulonephritis worldwide. (PubMed)

Hypothesis: dysregulation of immunologic balance resulting from hygiene and socioeconomic factors may influence the epidemiology and cause of glomerulonephritis worldwide. Glomerular diseases show diverse epidemiological characteristics throughout the world, which has been suggested to be caused by differences in genetics of the underlying populations or environmental exposure to the putative antigens or agents that either trigger or induce the disease. Recently, an alteration in immune balance (...) that this imbalance may help explain the predilection for membranoproliferative glomerulonephritis (GN) and mesangial proliferative GN to be associated with developing and/or poor nations, whereas immunoglobulin A nephropathy and minimal change disease are observed more commonly in industrialized nations. The implication of the Hygiene Hypothesis is that clinical expression of immune-mediated renal disease would depend on the prevailing T(H)1/T(H)2 balance, rather than the etiologic agent, and it may help explain

2003 American Journal of Kidney Diseases

2132. Characterization of the T-cell epitope that causes anti-GBM glomerulonephritis. (PubMed)

Characterization of the T-cell epitope that causes anti-GBM glomerulonephritis. We have demonstrated that a single T-cell epitope pCol(28-40) (SQTTANPSCPEGT) alone, which is derived from NC1 domain of alpha3 chain of type IV collagen (Col4alpha3 NC1), can induce severe glomerulonephritis in Wistar Kyoto rats. This study further characterized this T-cell epitope.A series of synthetic peptides derived from pCol (28-40) were tested in vivo and in vitro for their T-cell epitope activity (...) and nephritogenicity. Major histocompatability complex (MHC) class II molecules in Wistar Kyoto rats were cloned, and MHC restriction of pCol(28-40) was determined.The T-cell epitope pCol(28-40) was restricted by rat MHC class II RT.1Bl. Ten amino acid residues (29 to 38) were mapped to be the minimum core of the T-cell epitope, which was capable of inducing the T-cell response and severe glomerulonephritis. Only three residues were identified as absolutely critical for the T-cell epitope: position 31 (T

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2005 Kidney International

2133. Necrotizing glomerulonephritis caused by Bartonella henselae endocarditis. (PubMed)

Necrotizing glomerulonephritis caused by Bartonella henselae endocarditis. Glomerulonephritis secondary to endocarditis is uncommon and usually associated with valvular infection by blood culture-positive bacteria. We report 3 cases of necrotizing glomerulonephritis associated with culture-negative endocarditis caused by Bartonella henselae. Two of the patients presented with renal abnormalities and were investigated for endocarditis after results of renal biopsy. All 3 patients had an immune (...) surgery. The 2 patients who underwent cardiac surgery were discharged from the hospital with stable renal function. The third patient died 4 months after hospital admission of renal failure. In conclusion, glomerulonephritis caused by B henselae endocarditis is an immune complex-mediated disease characterized by segmental necrotizing and crescentic glomerular lesions that can respond to aggressive medical and surgical therapy.

2004 American Journal of Kidney Diseases

2134. Regional program for the study of glomerulonephritis. Central Committee of the Toronto Glomerulonephritis Registry. (PubMed)

. Randomized controlled trials of different types of therapy for five types of glomerulonephritis have been started under the coordination of the central registry. In view of the registry's low cost and high potential benefit, greater support for such projects is needed. Other centres should consider establishing similar registries to promote more rapid collection of cases and thus allow better evaluation of the development and treatment of this major cause of renal failure. (...) Regional program for the study of glomerulonephritis. Central Committee of the Toronto Glomerulonephritis Registry. The Toronto Glomerulonephritis Registry, a regional program for studying the natural history of the different types of glomerulonephritis and the effects of drug therapy on them, was established 6 years ago in Toronto. Data for all patients with histologic evidence of glomerulonephritis seen at the 16 participating hospitals are collected on standard forms and stored in a computer

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1981 Canadian Medical Association journal

2135. Functional Loss of ABCA1 in Mice Causes Severe Placental Malformation, Aberrant Lipid Distribution, and Kidney Glomerulonephritis As Well As High-Density Lipoprotein Cholesterol Deficiency (PubMed)

Functional Loss of ABCA1 in Mice Causes Severe Placental Malformation, Aberrant Lipid Distribution, and Kidney Glomerulonephritis As Well As High-Density Lipoprotein Cholesterol Deficiency Tangier disease (TD) and familial HDL deficiency (FHA) have recently been linked to mutations in the human ATP-binding cassette transporter 1 (hABCA1), a member of the ABC superfamily. Both diseases are characterized by the lowering or lack of high-density lipoprotein cholesterol (HDL-C) and low serum (...) -/- animals develop membranoproliferative glomerulonephritis due to deposition of immunocomplexes followed by cardiomegaly with ventricular dilation and hypertrophy, ultimately succumbing to congestive heart failure. This murine model of TD will be very useful in the study of lipid metabolism, renal inflammation, and cardiovascular disease and may reveal previously unsuspected relationships between them.

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2000 The American journal of pathology

2136. Antineutrophil cytoplasmic autoantibodies specific for myeloperoxidase cause glomerulonephritis and vasculitis in mice (PubMed)

Antineutrophil cytoplasmic autoantibodies specific for myeloperoxidase cause glomerulonephritis and vasculitis in mice Antineutrophil cytoplasmic autoantibodies (ANCAs) are identified in the circulation of approximately 80% of patients with pauci-immune necrotizing and crescentic glomerulonephritis and systemic small vessel vasculitis, such as microscopic polyangiitis and Wegener granulomatosis. The most common antigen target for ANCAs is myeloperoxidase (MPO), which is found in neutrophils (...) of glomerular Ig deposition. Thus, anti-MPO IgG alone was able to cause pauci-immune glomerular necrosis and crescent formation in the absence of functional T or B lymphocytes in Rag2(-/-) mice and in the presence of an intact immune system in wild-type C57BL/6J mice. This animal model offers strong support for a direct pathogenic role for ANCA IgG in human glomerulonephritis and vasculitis.

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2002 The Journal of clinical investigation

2137. Effect of diagnostic delay on disease severity and outcome in glomerulonephritis caused by anti-neutrophil cytoplasmic antibodies. (PubMed)

Effect of diagnostic delay on disease severity and outcome in glomerulonephritis caused by anti-neutrophil cytoplasmic antibodies. To measure the time between onset of symptoms and intention to treat in patients with anti-neutrophil cytoplasmic antibody (ANCA) associated glomerulonephritis; and to investigate the effect of any delay in diagnosis on disease severity at presentation and outcome.All ANCA positive patients with biopsy proven glomerulonephritis presenting in the North West Region (...) dialysis independent at final follow up.Prolonged delay in diagnosis of ANCA associated glomerulonephritis is associated with an increased risk of end stage renal failure.

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1996 Journal of Clinical Pathology

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