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Glomerulonephritis Causes

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181. Bacterial infection-related glomerulonephritis in adults. Full Text available with Trip Pro

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

2013 Kidney International

182. The role of macrophages in the fibrotic phase of rat crescentic glomerulonephritis. Full Text available with Trip Pro

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.

2013 American Journal of Physiology. Renal physiology

183. 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

184. 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

185. 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

186. Fibrillary glomerulonephritis: presenting as crescentic glomerulonephritis causing rapidly progressive renal failure Full Text available with Trip Pro

Fibrillary glomerulonephritis: presenting as crescentic glomerulonephritis causing rapidly progressive renal failure We report an unusual case of fibrillary glomerulonephritis (FGN) presenting as rapidly progressive renal failure and extensive crescent formation along with linear staining of capillary walls of the glomeruli on immunofluorescence, mimicking anti-glomerular basement membrane (anti-GBM) antibody-mediated disease. Laboratory results for circulating anti-GBM antibodies were negative (...) . The subsequent electron microscopic findings were that of presence of electron-dense deposits in the glomerular mesangium and capillary walls, comprising of non-branching fibrils with an average diameter of 16 nm consistent with a diagnosis of FGN. This case illustrates the crucial role of electron microscopy in differential diagnosis of crescentic glomerulonephritis.

2011 NDT Plus

187. The Role of Nephritis-Associated Plasmin Receptor (NAPlr) in Glomerulonephritis Associated with Streptococcal Infection Full Text available with Trip Pro

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

2012 Journal of Biomedicine and Biotechnology

188. MPO-ANCA associated crescentic glomerulonephritis with numerous immune complexes: case report. Full Text available with Trip Pro

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

2012 BMC Nephrology

189. Membranoproliferative glomerulonephritis complicating Waldenström's macroglobulinemia. Full Text available with Trip Pro

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

2012 BMC Nephrology

190. Renal biopsy in very elderly patients: data from the Spanish Registry of Glomerulonephritis. Full Text available with Trip Pro

) was the main indication for biopsy (47%), followed by nephrotic syndrome (32%). Amyloidosis was the most common histological diagnosis (16.9%), followed by crescentic glomerulonephritis type 3 associated with systemic vasculitis (14.1%). When histological findings were correlated with clinical syndromes, we found that amyloidosis was the leading cause of AKI (18.8%), and also the main determinant of nephrotic syndrome, with the same frequency as membranous nephropathy (22%). Crescentic glomerulonephritis (...) Renal biopsy in very elderly patients: data from the Spanish Registry of Glomerulonephritis. Studies on renal histology results in very elderly patients are extremely rare.We analyzed histology and clinical findings in patients aged over 85 years undergoing renal biopsy and whose data were included in the Spanish Registry of Glomerulonephritis between 1994 and 2009.A total of 17,680 native kidney biopsies were taken: 71 (0.4%) were from patients aged over 85 years. Acute kidney injury (AKI

2012 American journal of nephrology

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

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

192. Idiopathic membranoproliferative glomerulonephritis: does it exist? Full Text available with Trip Pro

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

2012 Transplantation

193. Acute Presentation and Persistent Glomerulonephritis Following Streptococcal Infection in a Patient With Heterozygous Complement Factor H-Related Protein 5 Deficiency. Full Text available with Trip Pro

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

2012 American Journal of Kidney Diseases

194. Association of a Novel Complement Factor H Mutation With Severe Crescentic and Necrotizing Glomerulonephritis. Full Text available with Trip Pro

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

2012 American Journal of Kidney Diseases

195. C3 glomerulonephritis and CFHR5 nephropathy. Full Text available with Trip Pro

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

2012 Transplantation

196. GLOMERULONEPHRITIS PRODUCED IN DOGS BY SPECIFIC ANTISERA : I. THE COURSE OF THE DISEASE RESULTING FROM INJECTION OF RABBIT ANTIDOG-PLACENTA SERUM OR RABBIT ANTIDOG-KIDNEY SERUM Full Text available with Trip Pro

GLOMERULONEPHRITIS PRODUCED IN DOGS BY SPECIFIC ANTISERA : I. THE COURSE OF THE DISEASE RESULTING FROM INJECTION OF RABBIT ANTIDOG-PLACENTA SERUM OR RABBIT ANTIDOG-KIDNEY SERUM The injection of rabbit antidog-placenta serum in 11 dogs resulted in an acute nephritis which was fatal within a month in 4, progressed to a chronic disease in 5, and healed in 2 animals. The nephritis produced in 5 dogs by the injection of rabbit antidog-kidney serum was comparable to that following the injection (...) of antiplacenta serum. The manifestations of the acute disease included edema, hypertension, proteinuria, cylindruria, hematuria, nitrogen retention, hypoalbuminemia, hypercholesterolemia, increased erythrocyte sedimentation rate, and anemia. The non-fatal chronic nephritis was characterized by proteinuria, cylindruria, and hematuria. With the onset of renal failure elevation of the blood urea nitrogen again occurred. Antiplacenta serum did not cause abortion when injected into pregnant dogs, nor did

1955 The Journal of experimental medicine

197. Functional adaptation of nephrons in dogs with acute progressing to chronic experimental glomerulonephritis. Full Text available with Trip Pro

Functional adaptation of nephrons in dogs with acute progressing to chronic experimental glomerulonephritis. Although a diminished fractional excretion of sodium (FENa) is the hallmark of acute proliferative glomerulonephritis (APGN), an enhanced natriuresis per glomerular filtration rate (GFR) in the chronic phases of this disease has been reported. We studied this adaptive response utilizing two different split-bladder dog models with unilateral, and a third group of dogs with bilateral (...) Masugi's nephritis. Group I. Six dogs with unilateral nonaccelerated APGN studied a mean of 6 days after induction had a mean base-line APGN/intact kidney GFR of 31/50 ml/min (P less than 0.005) and FENa of 0.2/0.75% (P less than 0.005). Acute volume expansion caused a smaller absolute increase in FENa from the APGN kidney, 1.6%, than from the intact kidney, 4.0%, (P less than 0.01). Maximum tubular secretion of rho-aminohippuric acid/GFR (TmPAH/GFR) measured in three dogs was higher in the APGN kidney

1976 Journal of Clinical Investigation

198. Glomerulonephritis with γ- and β1C-Globulin Deposits Induced in Rats by Mercuric Chloride Full Text available with Trip Pro

Glomerulonephritis with γ- and β1C-Globulin Deposits Induced in Rats by Mercuric Chloride Repeated subcutaneous injections of 0.15 or 0.25 mg/100 g of body weight of HgCl(2) may induce a membranous glomerulonephritis in rats. This glomerulonephritis with subepithelial deposits is similar, by electron microscopy and immunohistochemistry, to experimental chronic glomerulonephritis caused by immune complexes and to the human membranous glomerulonephritis.

1971 The American journal of pathology

199. Evidence for a pathogenic role of a cell-mediated immune mechanism in experimental glomerulonephritis Full Text available with Trip Pro

Evidence for a pathogenic role of a cell-mediated immune mechanism in experimental glomerulonephritis Lewis rats were injected intravenously with rabbit anti-rat glomerular basement membrane (GBM) antisera in doses that were sufficient to cause glomerular fixation of rabbit gamma globulin (RGG) detectable by immunofluorescence, but which failed to induce histologically detectable lesions. 24 h later, groups of rats received lymph node cells or serum from syngeneic donors that had been immunized

1978 The Journal of experimental medicine

200. EXPERIMENTAL ALLERGIC GLOMERULONEPHRITIS INDUCED IN THE RABBIT WITH HOMOLOGOUS RENAL ANTIGENS Full Text available with Trip Pro

EXPERIMENTAL ALLERGIC GLOMERULONEPHRITIS INDUCED IN THE RABBIT WITH HOMOLOGOUS RENAL ANTIGENS Rabbits immunized to several homologous renal antigens developed a variety of autoantikidney antibodies. Some of these antibodies reacted with the host's glomeruli and appeared to cause glomerulonephritis. Passive transfer of sera from some of these nephritic rabbits into normal, unilaterally nephrectomized rabbits led to the induction of nephritis. The production of autoantibody to glomeruli

1967 The Journal of experimental medicine

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