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Glomerulonephritis Causes

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181. The role of macrophages in the fibrotic phase of rat crescentic glomerulonephritis. (PubMed)

The role of macrophages in the fibrotic phase of rat crescentic glomerulonephritis. The ability of macrophages to cause acute inflammatory glomerular injury is well-established; however, the role of macrophages in the fibrotic phase of chronic kidney disease remains poorly understood. This study examined the role of macrophages in the fibrotic phase (days 14 to 35) of established crescentic glomerulonephritis. Nephrotoxic serum nephritis (NTN) was induced in groups of eight Wistar-Kyoto rats (...) against further peritubular capillary loss. However, sustained proteinuria, tubular damage, and interstitial T cell infiltration and activation were unaffected. In conclusion, this study demonstrates that macrophages contribute to renal dysfunction and tissue damage in established crescentic glomerulonephritis as it progresses from the acute inflammatory to a chronic fibrotic phase.

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2013 American Journal of Physiology. Renal physiology

182. Predictors for outcomes in patients with severe ANCA-associated glomerulonephritis who were dialysis-dependent at presentation: a study of 89 cases in a single Chinese center. (PubMed)

Predictors for outcomes in patients with severe ANCA-associated glomerulonephritis who were dialysis-dependent at presentation: a study of 89 cases in a single Chinese center. Anti-neutrophilcytoplasmic autoantibody (ANCA)-associated vasculitis may cause rapid deterioration of renal function, resulting in high prevalence of end-stage renal disease and mortality. The current study investigated factors associated with restoration of renal function and early mortality in patients with severe ANCA (...) ) and therapy-related death (P=0.037 and P=0.043, respectively).Among patients with severe ANCA-associated glomerulonephritis who were dialysis-dependent at presentation, those with a higher percentage of normal glomeruli and less extent of tubular atrophy/interstitial fibrosis have more chance of restoration of renal function. Increased risk for all-cause death and therapy-related death appears to be older age and pulmonary hemorrhage.Copyright © 2013 Elsevier Inc. All rights reserved.

2013 Seminars in arthritis and rheumatism

183. Recurrent gastrointestinal bleeding with ANCA associated glomerulonephritis successfully treated by transarterial embolization (PubMed)

Recurrent gastrointestinal bleeding with ANCA associated glomerulonephritis successfully treated by transarterial embolization Anti-neutrophil cytoplasmic antibody-associated vasculitis (AAV) is a group of autoimmune diseases that normally affects multiple organs. Recurrent gastrointestinal (GI) bleeding, a critical complication of AAV, remains a challenge. Here, we report a case of AAV complicated by pulmonary hemorrhage, severe recurrent gastrointestinal bleeding, and rapid progressive renal (...) insufficiency that was treated successfully with selective transarterial embolization, continuous veno-venous hemofiltration, plasma exchange, intravenous gamma globulin infusion, followed by steroids and cytotoxic drug therapy. We report this case considering that selective transarterial embolization may be a safe and effective alternative method in recurrent AAV associated GI bleeding caused by AAV refractory to medical therapy.

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2013 Pakistan Journal Of Medical Sciences

184. Bacterial infection-related glomerulonephritis in adults. (PubMed)

the elderly and diabetics, do not recover renal function. Whereas the pathogenesis of post-streptococcal glomerulonephritis has been studied extensively, leading to the identification of two candidate nephritogenic streptococcal antigens, glyceraldehyde-3-phosphate dehydrogenase and pyrogenic exotoxin B, few investigations have focused on IRGN caused by other bacteria. This review will address the current status of sporadic bacterial IRGN in adults. (...) Bacterial infection-related glomerulonephritis in adults. In the past, most cases of bacterial infection-related glomerulonephritis (IRGN) occurred in children following streptococcal upper respiratory tract or skin infections and were called postinfectious GN. Over the past 3 decades, there has been an important shift in epidemiology, bacteriology, and outcome of IRGN. A significant percentage of cases now target adults, particularly the elderly or immunocompromised. Because adult infections

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2013 Kidney International

185. MPO-ANCA associated crescentic glomerulonephritis with numerous immune complexes: case report. (PubMed)

MPO-ANCA associated crescentic glomerulonephritis with numerous immune complexes: case report. Antineutrophil cytoplasmic antibody (ANCA)-associated crescentic glomerulonephritis (CGN) is a major cause of rapidly progressive glomerulonephritis (RPGN). ANCA-associated CGN is generally classified into pauci-immune RPGN, in which there are few or no immune complexes.A 78-year-old man presented with RPGN after a 7-year course of chronic proteinuria and hematuria with stable renal function. A blood (...) examination showed a high titer of myeloperoxidase (MPO)-ANCA. A renal biopsy showed crescentic glomerulonephritis with abundant subepithelial, intramenbranous and subendothelial deposits by electron microscopy, leading to the diagnosis of ANCA-associated CGN superimposed on type 3 membranoproliferative glomerulonephritis (MPGN).This case is unique in that type 3 MPGN and MPO-ANCA-associated CGN coexisted, and no similar case has been reported to date. Because ANCA-associated CGN has a predilection

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2012 BMC Nephrology

186. Membranoproliferative glomerulonephritis complicating Waldenström's macroglobulinemia. (PubMed)

Membranoproliferative glomerulonephritis complicating Waldenström's macroglobulinemia. Lymphoproliferative disorders causing paraproteinemia can be associated with various kidney injuries including the deposition of monoclonal immunoglobulins (Ig). A known glomerular manifestation of Waldenström's macroglobulinemia is characterized by prominent intracapillary hyaline thrombi and lack of conspicuous glomerular proliferation. The present case was special in 2 aspects: 1. the diagnosis (...) of glomerulonephritis was unexpected before renal biopsy, 2. the prominent glomerular proliferation paired with large intracapillary hyaline thrombi is uncommon in Waldenström's macroglobulinemia-associated glomerulonephritis.A 73-year-old Caucasian woman with a long-standing history of rheumatoid arthritis and Waldenström's macroglobulinemia was admitted for acute renal failure (ARF), which initially was presumed to be the consequence of extrarenal causes. Proteinuria and hematuria were only mild. In renal core

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2012 BMC Nephrology

187. Acute Presentation and Persistent Glomerulonephritis Following Streptococcal Infection in a Patient With Heterozygous Complement Factor H-Related Protein 5 Deficiency. (PubMed)

Acute Presentation and Persistent Glomerulonephritis Following Streptococcal Infection in a Patient With Heterozygous Complement Factor H-Related Protein 5 Deficiency. Acute poststreptococcal glomerulonephritis is a common cause of acute nephritis in children. Transient hypocomplementemia and complete recovery are typical, with only a minority developing chronic disease. We describe a young girl who developed persistent kidney disease and hypocomplementemia after a streptococcal throat

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2012 American Journal of Kidney Diseases

188. Association of a Novel Complement Factor H Mutation With Severe Crescentic and Necrotizing Glomerulonephritis. (PubMed)

by oral steroids resulted in symptom alleviation and improved kidney function. This case shows what is to our knowledge a unique and previously unpublished cause of severe crescentic and necrotizing glomerulonephritis. Furthermore, the case demonstrates an expanding spectrum of complement-mediated glomerulonephritis and shows that crescentic and necrotizing glomerulonephritis with solely complement deposits should be evaluated for abnormalities in the alternative pathway of complement.Copyright © 2012 (...) Association of a Novel Complement Factor H Mutation With Severe Crescentic and Necrotizing Glomerulonephritis. Severe crescentic and necrotizing glomerulonephritis typically is associated with anti-glomerular basement membrane or antineutrophil cytoplasmic antibodies. In this report, we describe a 23-year-old man with severe crescentic and necrotizing glomerulonephritis. Both anti-glomerular basement membrane and antineutrophil cytoplasmic antibody titers were negative. Kidney biopsy showed

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2012 American Journal of Kidney Diseases

189. Idiopathic membranoproliferative glomerulonephritis: does it exist? (PubMed)

showing glomerulonephritis has diminished over time. In the modern era, MPGN is mainly classified morphologically on the basis of immunoglobulin (Ig; monoclonal or polyclonal) and complement (C3 only or combined with Ig) deposition and secondarily on the basis of its appearance on ultra-structural examination. Idiopathic MPGN is a diagnosis of exclusion, at least in many adults and a portion of children, and a systematic approach to evaluation will often uncover a secondary cause, such as an infection (...) Idiopathic membranoproliferative glomerulonephritis: does it exist? When membranoproliferative glomerulonephritis (MPGN) was first delineated as a discrete clinico-pathological entity more than a half-century ago, most cases were regarded as idiopathic (or primary) in nature. Advances in analysis of pathogenetic mechanisms and etiologies underlying the lesion of MPGN have radically altered the prevalence of the truly idiopathic form of MPGN. In addition, MPGN as a category among renal biopsies

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2012 Transplantation

190. C3 glomerulonephritis and CFHR5 nephropathy. (PubMed)

C3 glomerulonephritis and CFHR5 nephropathy. Complement is an important aspect of defence against infection and its activation and regulation are finely balanced. Disordered complement regulation can lead to C3 glomerulonephritis (C3GN), which is characterized by complement (but not immunoglobulin) deposition in the glomerulus of the kidney. Although only recently recognized as a clinical entity, C3GN is important and elucidation of its molecular causes, by studies of single cases and families (...) , has identified key proteins that protect the kidney from complement-mediated damage. The commonest cause of C3GN is complement factor H-related 5 (CFHR5) nephropathy, which is endemic in Greek Cypriots. Genetic evidence implicates some of the same complement regulators in the aetiology of common immune complex glomerular disorders such as IgA nephropathy and lupus nephritis. Importantly, therapeutic manipulation of the complement pathway is now feasible. An exciting challenge is to determine

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2012 Transplantation

191. The Role of Nephritis-Associated Plasmin Receptor (NAPlr) in Glomerulonephritis Associated with Streptococcal Infection (PubMed)

The Role of Nephritis-Associated Plasmin Receptor (NAPlr) in Glomerulonephritis Associated with Streptococcal Infection It is well known that glomerulonephritis can occur after streptococcal infection, which is classically referred to as acute poststreptococcal glomerulonephritis (APSGN). The pathogenic mechanism of APSGN has been described by so-called immune complex theory, which involves glomerular deposition of nephritogenic streptococcal antigen and subsequent formation of immune complexes (...) in situ and/or the deposition of circulating antigen-antibody complexes. However, the exact entity of the causative antigen has remained a matter of debate. We isolated a nephritogenic antigen for APSGN from the cytoplasmic fractions of group A streptococcus (GAS) depending on the affinity for IgG of APSGN patients. The amino acid and the nucleotide sequences of the isolated protein revealed to be highly identical to those of reported plasmin(ogen) receptor of GAS. Thus, we termed this antigen

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2012 Journal of Biomedicine and Biotechnology

192. Acute Glomerulonephritis

Glomerulonephritis Aka: Acute Glomerulonephritis , Glomerulonephritis From Related Chapters II. Definition with casts III. Causes See ( , ) Membranous Glomerulonephritis ( ) Nephritis with low complement Postinfectious proliferative Glomerulonephritis (classic) Membranoproliferative Glomerulonephritis Cryoglobulinemia Nephritis with normal complement IgA Nephropathy (Berger's Disease) Fibrillary Glomerulonephritis Renal Wegner's Granulomatosis IV. Symptoms (variably present) Malaise Low grade fever V. Symptoms (...) Treat specific cause Images: Related links to external sites (from Bing) These images are a random sampling from a Bing search on the term "Acute Glomerulonephritis." Click on the image (or right click) to open the source website in a new browser window. Related Studies (from Trip Database) Ontology: Glomerulonephritis (C0017658) Definition (NCI) A renal disorder characterized by damage in the glomeruli. It may be acute or chronic, focal or diffuse, and it may lead to renal failure. Causes include

2015 FP Notebook

193. Poststreptococcal Glomerulonephritis

Poststreptococcal Glomerulonephritis Poststreptococcal Glomerulonephritis Aka: Poststreptococcal Glomerulonephritis , Post-Streptococcal Glomerulonephritis , Acute post-streptococcal glomerulonephritis From Related Chapters II. Epidemiology Previously, most common cause of , but has decreased significantly in the U.S. As of 2018, most cases occur in underserved regions Previously most often in childhood (ages 2 to 6) Now more common in age >60 years old, especially with comorbidities III. Pathophysiology (...) Poststreptococcal Glomerulonephritis Poststreptococcal Glomerulonephritis Toggle navigation Brain Head & Neck Chest Endocrine Abdomen Musculoskeletal Skin Infectious Disease Hematology & Oncology Cohorts Diagnostics Emergency Findings Procedures Prevention & Management Pharmacy Resuscitation Trauma Emergency Procedures Ultrasound Cardiovascular Emergencies Lung Emergencies Infectious Disease Pediatrics Neurologic Emergencies Skin Exposure Miscellaneous Abuse Cancer Administration 4

2015 FP Notebook

194. Rapidly Progressive Glomerulonephritis

Progressive Glomerulonephritis Rapidly Progressive Glomerulonephritis Aka: Rapidly Progressive Glomerulonephritis , RPGN From Related Chapters II. Causes III. Symptoms and Signs Similar to Rapidly Progressive IV. Diagnosis: Renal Biopsy Crescentic V. Course Progresses to within weeks to months Patients refusing within 6 months: 50% VI. Management d dose glucocorticoids Cytotoxic agents Cyclophosphamide Plasma exchange Images: Related links to external sites (from Bing) These images are a random sampling (...) Rapidly Progressive Glomerulonephritis Rapidly Progressive Glomerulonephritis Toggle navigation Brain Head & Neck Chest Endocrine Abdomen Musculoskeletal Skin Infectious Disease Hematology & Oncology Cohorts Diagnostics Emergency Findings Procedures Prevention & Management Pharmacy Resuscitation Trauma Emergency Procedures Ultrasound Cardiovascular Emergencies Lung Emergencies Infectious Disease Pediatrics Neurologic Emergencies Skin Exposure Miscellaneous Abuse Cancer Administration 4 Rapidly

2015 FP Notebook

195. Impact of Posttransplantation Glomerulonephritis on Long-term Outcome of Kidney Transplants: Single-Center 20-Year Experience. (PubMed)

and recurrent glomerulonephritis are major causes of long-term allograft loss. However, data regarding the long-term impact of posttransplantation glomerulonephritis (PTGN) on ethnic Chinese populations are still unavailable.From 1984 to 2010, a total of 268 patients who underwent renal allograft biopsies were reviewed retrospectively. Renal outcomes were compared by Kaplan-Meier analysis, and risk factors for renal survival and all-cause mortality were analyzed using the Cox proportional hazards model.In (...) Impact of Posttransplantation Glomerulonephritis on Long-term Outcome of Kidney Transplants: Single-Center 20-Year Experience. Successful renal transplantation has been performed in patients with end-stage renal disease and has been routine in patients with end-stage renal failure for more than two decades. Despite advances in the use of immunosuppressants, there has been only modest improvement in long-term allograft survival. Accumulating data have demonstrated that chronic rejection

2012 World Journal of Surgery

196. Strain differences and the genetic basis of experimental autoimmune anti-glomerular basement membrane glomerulonephritis (PubMed)

Strain differences and the genetic basis of experimental autoimmune anti-glomerular basement membrane glomerulonephritis Goodpasture's, or anti-glomerular basement membrane (GBM), disease presents with rapidly progressive glomerulonephritis, caused by autoimmunity to a component of the GBM, the non-collagenous domain of the α3 chain of type IV collagen [α3(IV)NC1]. To investigate the mechanisms of inflammation in glomerulonephritis and to test new approaches to treatment, animal models (...) of glomerulonephritis, termed experimental autoimmune glomerulonephritis (EAG), have been developed in susceptible strains of rats and mice. This review article describes how these models of EAG have been developed over the past three decades, discusses the evidence for the involvement of both humoral and cell-mediated immunity in the induction and pathogenesis of glomerulonephritis in these models and highlights recent, emerging data that have identified potential candidate genes that may control the genetic

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2011 International journal of experimental pathology

197. Multi-glycoside of Tripterygium wilfordii Hook. f. reduces proteinuria through improving podocyte slit diaphragm dysfunction in anti-Thy1.1 glomerulonephritis. (PubMed)

Multi-glycoside of Tripterygium wilfordii Hook. f. reduces proteinuria through improving podocyte slit diaphragm dysfunction in anti-Thy1.1 glomerulonephritis. Multi-glycoside of Tripterygium wilfordii Hook. f. (GTW) has been proved clinically effective in reducing proteinuria in chronic kidney disease in China. However, the mechanisms involved are still unclear. In this study we examined the effects of GTW at the different dosages on proteinuria and podocyte slit diaphragm (SD) dysfunction (...) in anti-Thy1.1 glomerulonephritis (GN).Rats with anti-Thy1.1 GN were divided into 2 groups, a GTW group and a vehicle group, and sacrificed at 30 min, on day 7, and on day 14 in Experiments 1, 2 and 3, respectively. The administration of GTW at the moderate and high doses was started 3 days before or at the same time of antibody injection till sacrifice. Proteinuria was determined in Experiments 1, 2, and 3. After sacrifice, the staining intensity of SD-associated key functional molecules including

2011 Journal of Ethnopharmacology

198. ANCA-Associated Glomerulonephritis in Systemic-Onset Juvenile Idiopathic Arthritis. (PubMed)

ANCA-Associated Glomerulonephritis in Systemic-Onset Juvenile Idiopathic Arthritis. Systemic-onset juvenile idiopathic arthritis is an inflammatory disease of unknown cause and is not commonly associated with kidney involvement. We describe 3 patients with systemic-onset juvenile idiopathic arthritis with high disease activity who developed antineutrophil cytoplasmic antibody (ANCA)-associated glomerulonephritis 1-6 years after the onset of systemic-onset juvenile idiopathic arthritis. Renal (...) and systemic-onset juvenile idiopathic arthritis remission occurred in one patient under anti-interleukin 1 (anti-IL-1) treatment associated with immunosuppressive drugs. The other 2 patients developed end-stage renal disease, and one of those patients died. This report suggests that the diagnosis of ANCA-associated glomerulonephritis must be considered in patients with systemic-onset juvenile idiopathic arthritis with persistently active systemic disease who present with proteinuria. Furthermore, use

2011 American Journal of Kidney Diseases

199. Allograft Failure in Kidney Transplant Recipients With Membranoproliferative Glomerulonephritis. (PubMed)

-disease recurrence failures (P < 0.001).Limited pretransplant clinical and biopsy data.A diagnosis of MPGN-I or MPGN-II has a significant negative impact on overall primary allograft survival compared with other forms of glomerulonephritis, whereas only MPGN-I has a significant, but modest, negative effect compared with other causes of end-stage renal disease.Copyright © 2011 National Kidney Foundation, Inc. Published by Elsevier Inc. All rights reserved. (...) Allograft Failure in Kidney Transplant Recipients With Membranoproliferative Glomerulonephritis. Membranoproliferative glomerulonephritis types I (MPGN-I) and II (MPGN-II) are rare diseases that in limited case series have been reported to recur frequently in kidney transplants and have a negative impact on allograft survival.Retrospective database review.189,211 primary kidney transplants in the United Network for Organ Sharing (UNOS) database from September 1987 to May 2007.MPGN-I (811

2011 American Journal of Kidney Diseases

200. Myeloperoxidase-Specific Plasma Cell Depletion by Bortezomib Protects from Anti-Neutrophil Cytoplasmic Autoantibodies-Induced Glomerulonephritis. (PubMed)

Myeloperoxidase-Specific Plasma Cell Depletion by Bortezomib Protects from Anti-Neutrophil Cytoplasmic Autoantibodies-Induced Glomerulonephritis. Anti-neutrophil cytoplasmic autoantibodies (ANCA) cause vasculitis and necrotizing crescentic glomerulonephritis (NCGN). Steroids and cytotoxic drugs reduce mortality but can cause significant adverse events. The proteasome inhibitor bortezomib (BTZ) prevents glomerulonephritis in mouse models of lupus but its efficacy in ANCA-associated (...) glomerulonephritis is unknown. We induced anti-MPO IgG-mediated NCGN by transplanting wild-type bone marrow (BM) into irradiated MPO-deficient mice immunized with MPO. Four weeks after BM transplantation, we treated mice with steroid/cyclophosphamide (S/CYC) or BTZ. Compared with untreated control mice, both S/CYC and BTZ significantly reduced urine abnormalities, NCGN, and infiltration of neutrophils and macrophages. Response to BTZ depended on timing of administration: BTZ abrogated NCGN if begun 3 weeks

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2011 Journal of the American Society of Nephrology

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