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Glomerulonephritis Causes

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2121. Up-regulation of cytokines in glomerulonephritis associated with murine malaria infection Full Text available with Trip Pro

Up-regulation of cytokines in glomerulonephritis associated with murine malaria infection Malaria infections often cause glomerulonephritis (GN), and multiple factors have been implicated in the pathogenesis of glomerular injury. The role of cytokines in malaria associated glomerulonephritis has not been clearly defined. To study the importance of cytokines in malarial nephritis, we investigated the expression of tumour necrosis factor-alpha (TNF-alpha), interleukin-1alpha (IL-1alpha), IL-6, IL (...) with the severity of proteinuria. Our findings show that there is up-regulation of cytokines in the pathogenesis of glomerulonephritis associated with murine malaria infection.

1999 International journal of experimental pathology

2122. Post-streptococcal glomerulonephritis in Hong Kong. Full Text available with Trip Pro

Post-streptococcal glomerulonephritis in Hong Kong. Of 74 paediatric inpatients with acute glomerulonephritis, 58 (78%) had a raised (greater than 1/200) antistreptolysin O titre. Serum C3 concentration was low in 73, but returned to normal within six weeks. Streptococcal infection remains the commonest cause of acute nephritis in children in Hong Kong, possibly due to overcrowded living conditions.

1987 Archives of Disease in Childhood

2123. Angiotensin-converting enzyme inhibition and the combination of a beta blocker and a diuretic are equally effective in lowering proteinuria in patients with glomerulonephritis. (Abstract)

Angiotensin-converting enzyme inhibition and the combination of a beta blocker and a diuretic are equally effective in lowering proteinuria in patients with glomerulonephritis. In this study we compared the antihypertensive and antiproteinuric efficacies of an angiotensin-converting enzyme inhibitor and of conventional treatment consisting of a beta blocker and a diuretic in 13 patients with biopsy-proven glomerulonephritis and a proteinuria of more than 2 g/24 h. Ten of these 13 patients were (...) respectively. Both treatment modalities caused similar reductions in proteinuria, being 3.4 g/24 h (mean, 95% confidence interval 2.1-4.8) on benazepril and 3.2 (1.2-5.1) g/24 h on metoprolol/chlorthalidone. Glomerular filtration rate and renal plasma flow were slightly less during metoprolol/chlorthalidone treatment. Subgroup analysis of normotensive patients gave similar results. In conclusion, in these patients with glomerular disease angiotensin-converting enzyme inhibition was not more effective than

1993 Nephrology, dialysis, transplantation : official publication of the European Dialysis and Transplant Association - European Renal Association Controlled trial quality: uncertain

2124. Short-term effect of vitamin K administration on prednisolone-induced loss of bone mineral density in patients with chronic glomerulonephritis. (Abstract)

Short-term effect of vitamin K administration on prednisolone-induced loss of bone mineral density in patients with chronic glomerulonephritis. Glucocorticoid-induced osteoporosis has been reported to be caused by enhanced bone resorption and suppressed bone formation. To clarify whether administration of vitamin K, which enhances bone formation, prevents prednisolone-induced loss of bone mineral density (BMD), a randomized, prospective, controlled study was conducted on 20 patients (...) with chronic glomerulonephritis scheduled for treatment with prednisolone. All patients were initially treated with 0.8 mg/kg body weight/day of prednisolone (maximum of 40 mg) for 4 weeks, tapering to 20 mg/day over approximately 6 weeks. Ten patients received prednisolone alone (Group 1), and the other 10 patients received prednisolone plus 15 mg of menatetrenone, vitamin K, three times per day (Group 2). BMD of the lumbar spine measured by dual-energy X-ray absorptiometry (DXA) and biochemical markers

2000 Calcified tissue international Controlled trial quality: uncertain

2125. Renoprotective effect of small doses of losartan and enalapril in patients with primary glomerulonephritis. Short-term observation. (Abstract)

-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 Controlled trial quality: uncertain

2126. Immunodominant epitopes of alpha3(IV)NC1 induce autoimmune glomerulonephritis in rats. Full Text available with Trip Pro

antibody binding, also induces glomerulonephritis in rats. The middle third of alpha3(IV)NC1 does not induce glomerulonephritis but appears to enhance disease with the amino terminal third. Finally, the presence of the collagen X leader sequence appears to convey greater nephritogenicity. These studies suggest that not only the nephritogenic epitope itself, but flanking sequences and the conformational context of the nephritogenic epitope may influence its ability to cause glomerulonephritis. (...) Immunodominant epitopes of alpha3(IV)NC1 induce autoimmune glomerulonephritis in rats. The major Goodpasture antibody binding epitopes have been localized to the amino-terminal third of the noncollagenous domain (NC1) of the alpha3 chain of type IV collagen [alpha3(IV)NC1]. The present study determined whether the same epitopes induce glomerulonephritis in rats.We immunized Wistar Kyoto (WKY) rats with human alpha3(IV)/alpha1(IV)NC1 chimeric proteins or full-length recombinant alpha3(IV)NC1

2003 Kidney International

2127. Membranoproliferative glomerulonephritis develops in a child with autologous stem cell transplant. (Abstract)

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

2128. IgA antiglomerular basement membrane nephritis associated with Crohn's disease: a case report and review of glomerulonephritis in inflammatory bowel disease. (Abstract)

gangrene of the distal upper and lower limbs. The patient did not respond to plasmapheresis and steroid therapy and died of upper gastrointestinal bleeding. Renal tissue obtained at autopsy showed IgA-mediated antiglomerular basement membrane crescentic glomerulonephritis. Linear staining of the glomerular basement membrane by non-IgG antibodies is quite unusual with only 11 cases previously reported in the worldwide literature, 8 caused by IgA. Glomerulonephritis is a rarely reported extraintestinal (...) of the gastrointestinal disorder. The histologic findings were varied and included membranoproliferative glomerulonephritis, mesangioproliferative glomerulonephritis, membranous nephropathy, IgA nephropathy, and IgM nephropathy. Thus, the authors present the first case of glomerulonephritis caused by antiglomerular basement membrane disease in association with inflammatory bowel disease.

2003 American Journal of Kidney Diseases

2129. A novel mechanism of nephron loss in a murine model of crescentic glomerulonephritis. Full Text available with Trip Pro

A novel mechanism of nephron loss in a murine model of crescentic glomerulonephritis. Nephron loss is a major determinant of renal failure in glomerular diseases. The prevalent concept stresses the role of the toxicity of filtered proteins and/or of interstitial inflammation in tubular degeneration. However, whether that concept is compatible with the actual histopathological features of nephron loss has not been investigated specifically.We investigated the morphological aspects of tubular (...) degeneration in crescentic glomerulonephritis in mice. Glomerulonephritis was induced by intravenous injection of anti-glomerular basement membrane antiserum in presensitized mice. Kidneys were fixed by perfusion and examined by light- and electron microscopy and by immunohistochemistry.Tubular degeneration started with cellular hypotrophy in the proximal tubule. Hypotrophy appeared to follow obstruction of the initial proximal tubule by a cellular crescent. Whereas induction of intercellular adhesion

2003 Kidney International

2130. Glomerulonephritis and malignancy: a population-based analysis. Full Text available with Trip Pro

Glomerulonephritis and malignancy: a population-based analysis. An association between glomerulonephritis and malignant tumors has previously both been found and discarded in clinical series, but to our knowledge never has been tested in a population-based setting.The Danish Kidney Biopsy Registry includes all kidney biopsies performed from 1985. Using a unique personal identification number, each person in the registry to the National Population Registry and the Danish Cancer Registry were (...) represent a two- to threefold excess of the expected number at <1 and 1 to 4, but not >or=5 years after a biopsy. Non-Hodgkin's lymphomas were observed six to eight times more than expected. Cancer excess was seen in glomerulonephritides with a known or suspected virus etiology.The excess cancer rate could be the result of underlying undiagnosed tumors whose antigens have initiated glomerulonephritis, or the immunosuppressive therapy that initiated or energized tumor cells. Based on the findings in our

2003 Kidney International

2131. Plasminogen activator inhibitor-1 is a significant determinant of renal injury in experimental crescentic glomerulonephritis. (Abstract)

Plasminogen activator inhibitor-1 is a significant determinant of renal injury in experimental crescentic glomerulonephritis. Crescentic glomerulonephritis is characterized by glomerular fibrin deposition, and experimental crescentic glomerulonephritis has been shown to be fibrin-dependent. Net fibrin deposition is a balance between activation of the coagulation system causing glomerular fibrin deposition and fibrin removal by the plasminogen-plasmin (fibrinolytic) system. Plasminogen activator (...) inhibitor-1 (PAI-1) inhibits fibrinolysis by inhibiting plasminogen activators and has effects on leukocyte recruitment and matrix deposition. To test the hypothesis that the presence of PAI-1 and its levels were a determinant of injury in crescentic glomerulonephritis, accelerated anti-glomerular basement membrane glomerulonephritis was induced in mice genetically deficient in PAI-1 (PAI-1 -/-), PAI-1 heterozygotes (PAI-1 +/-), and mice engineered to overexpress PAI-1 (PAI-1 tg). Compared with strain

2003 Journal of the American Society of Nephrology

2132. Heterogeneity of antigen expression explains controversy over glomerular macrophage accumulation in mouse glomerulonephritis. (Abstract)

this apparent discrepancy.Kidneys were collected from normal mice and mice killed at 2 and 10 days after induction of accelerated anti-glomerular basement membrane (GBM) glomerulonephritis. Following fixation, macrophages were detected by immunoperoxidase staining in serial kidney sections using antibodies recognising CD11b, F4/80 and CD68.Induction of anti-GBM nephritis caused a progressive increase in glomerular and interstitial leukocytes. At days 2 and 10, there were more CD68+ macrophages in glomeruli (...) Heterogeneity of antigen expression explains controversy over glomerular macrophage accumulation in mouse glomerulonephritis. Many antibody labelling studies have suggested that there are few or no glomerular macrophages in mouse models of glomerulonephritis, despite the presence of a prominent interstitial macrophage infiltrate. These findings conflict with studies of human and rat glomerulonephritis. Therefore, we examined whether heterogeneity of macrophage antigen expression could explain

2003 Transplantation

2133. Glomerulonephritis in the vasculitides: advances in immunopathology. (Abstract)

Glomerulonephritis in the vasculitides: advances in immunopathology. Systemic vasculitis refers to a condition of blood vessel inflammation, of which the causes are various. In a substantial number of cases, autoantibodies against neutrophil cytoplasm constituents (ANCAs) are present. The authors then refer to the systemic vasculitis as ANCA-associated systemic vasculitis. Renal disease is an unfavorable component, leading to dialysis dependency in a considerable number of patients. This review

2003 Current Opinion in Rheumatology

2134. Necrotizing glomerulonephritis caused by Bartonella henselae endocarditis. (Abstract)

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

2135. Characterization of the T-cell epitope that causes anti-GBM glomerulonephritis. Full Text available with Trip Pro

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

2005 Kidney International

2136. Production of a novel class of polyreactive pathogenic autoantibodies in BXD2 mice causes glomerulonephritis and arthritis. (Abstract)

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

2006 Arthritis and Rheumatism

2137. Regional program for the study of glomerulonephritis. Central Committee of the Toronto Glomerulonephritis Registry. Full Text available with Trip Pro

. 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

1981 Canadian Medical Association journal Controlled trial quality: uncertain

2138. Antineutrophil cytoplasmic autoantibodies specific for myeloperoxidase cause glomerulonephritis and vasculitis in mice Full Text available with Trip Pro

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.

2002 The Journal of clinical investigation

2139. Functional Loss of ABCA1 in Mice Causes Severe Placental Malformation, Aberrant Lipid Distribution, and Kidney Glomerulonephritis As Well As High-Density Lipoprotein Cholesterol Deficiency Full Text available with Trip Pro

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.

2000 The American journal of pathology

2140. Effect of diagnostic delay on disease severity and outcome in glomerulonephritis caused by anti-neutrophil cytoplasmic antibodies. Full Text available with Trip Pro

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.

1996 Journal of Clinical Pathology

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