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Glomerulonephritis Causes

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81. Innate and adaptive immunity in experimental glomerulonephritis: a pathfinder tale. (PubMed)

Innate and adaptive immunity in experimental glomerulonephritis: a pathfinder tale. The role of innate and adaptive immune cells in the experimental model of nephrotoxic serum nephritis (NTS) has been rigorously studied in recent years. The model is dependent on kidney-infiltrating T helper (TH) 17 and TH1 cells, which recruit neutrophils and macrophages, respectively, and cause sustained kidney inflammation. In a later phase of disease, regulatory T cells (Tregs) infiltrate the kidney (...) capacity. Together, these two cell populations inhibit T cell differentiation and proliferation, thereby limiting disease activity by as yet unknown mechanisms. In contrast, the spleen plays no role in immune activation in NTS, but constitutes a place of extramedullary haematopoiesis. The complex interactions of immune cells in NTS are still under investigation and might ultimately lead to targeted therapies in glomerulonephritis.

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2016 Pediatric Nephrology

82. Bartonella Endocarditis and Pauci-Immune Glomerulonephritis: A Case Report and Review of the Literature (PubMed)

Bartonella Endocarditis and Pauci-Immune Glomerulonephritis: A Case Report and Review of the Literature Among culture-negative endocarditis in the United States, Bartonella species are the most common cause, with Bartonella henselae and Bartonella quintana comprising the majority of cases. Kidney manifestations, particularly glomerulonephritis, are common sequelae of infectious endocarditis, with nearly half of all Bartonella patients demonstrating renal involvement. Although a pauci-immune (...) pattern is a frequent finding in infectious endocarditis-associated glomerulonephritis, it is rarely reported in Bartonella endocarditis. Anti-neutrophil cytoplasmic antibody (ANCA) positivity can be seen with many pathogens causing endocarditis and has been previously reported with Bartonella species. In addition, ANCA-associated vasculitis can also present with renal and cardiac involvement, including noninfectious valvular vegetations and pauci-immune glomerulonephritis. Given the overlap

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2016 Infectious Diseases in Clinical Practice (Baltimore, Md.)

83. Central venous catheter infection-related glomerulonephritis under long-term parenteral nutrition: a report of two cases (PubMed)

under long-term parenteral nutrition who developed glomerulonephritis associated with central venous catheter infection. Persistent bacterial infection in indwelling medical devices placed in the blood-stream such as a ventricular-atrial shunt is known to cause glomerulonephritis, a condition termed shunt nephritis. We reported the clinical manifestations, treatment and their pathological findings in the two patients with glomerulonephritis associated with central venous catheter infection.Both (...) Central venous catheter infection-related glomerulonephritis under long-term parenteral nutrition: a report of two cases Advances in long-term parenteral nutrition via indwelling central venous catheter have improved the quality of life and mortality in patients with life-threatening gastrointestinal diseases complicated with severely impaired absorption. However, infection to central venous catheter is still a common and critical complication for such patients. We encountered two patients

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2016 BMC research notes

84. Small vessel microembolization and acute glomerulonephritis following infection of aesthetic filler implants (PubMed)

Small vessel microembolization and acute glomerulonephritis following infection of aesthetic filler implants The systemic consequences of esthetic filler injections are poorly understood.We report a patient with a past history of subcutaneous injection of aesthetic filler material in the lower legs, who presented with post-infectious glomerulonephritis following necrotic leg ulcers at the injection site. Kidney biopsy revealed the presence of translucent, non-birefringent microspherical bodies (...) and microembolization at the time of administration cannot be ruled out.In conclusion, aesthetic filler implants may cause microembolization into small vessels. Recognition of the characteristic morphology may expedite diagnosis and avoid unnecessary further testing.

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2016 Diagnostic pathology

85. Nephrotic Syndrome without Hematuria due to Infection-Related Glomerulonephritis Mimicking Minimal-Change Disease in a Child (PubMed)

observed electron-microscopically. These findings led to the diagnosis of nephrotic syndrome due to infection-related endocapillary proliferative glomerulonephritis, although the causative organism of his nephritis was not detected. He recovered with rest and dietary cure. When we examine an acute nephrotic child, infection-related glomerulonephritis should be considered as the differential diagnosis to avoid unnecessary use of corticosteroids. (...) Nephrotic Syndrome without Hematuria due to Infection-Related Glomerulonephritis Mimicking Minimal-Change Disease in a Child Nephrotic syndrome without hematuria due to infection-related glomerulonephritis is uncommon. The present report describes a case of nephrotic syndrome due to infection-related glomerulonephritis without hematuria and hypertension in an older child. A 14-year-old boy was referred to our hospital because of a 5-day history of fever, nausea, weight gain and recent leg edema

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2016 Case Reports in Nephrology and Dialysis

86. Cooperation of ETV6/RUNX1 and BCL2 enhances immunoglobulin production and accelerates glomerulonephritis in transgenic mice (PubMed)

Cooperation of ETV6/RUNX1 and BCL2 enhances immunoglobulin production and accelerates glomerulonephritis in transgenic mice The t(12;21) translocation generating the ETV6/RUNX1 fusion gene represents the most frequent chromosomal rearrangement in childhood leukemia. Presence of ETV6/RUNX1 alone is usually not sufficient for leukemia onset, and additional genetic alterations have to occur in ETV6/RUNX1-positive cells to cause transformation. We have previously generated an ETV6/RUNX1 transgenic (...) . This was associated with faster development of follicular B cell lymphoma and exacerbated immune complex glomerulonephritis. ETV6/RUNX1-BCL2 double transgenic animals displayed increased B cell numbers and immunoglobulin titers compared to Vav-BCL2 transgenic mice. This led to pronounced deposition of immune complexes in glomeruli followed by accelerated development of immune complex glomerulonephritis. Thus, our study reveals a previously unrecognized synergism between ETV6/RUNX1 and BCL2 impacting on malignant

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2016 Oncotarget

87. 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

2018 FP Notebook

88. 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

2018 FP Notebook

89. 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

2018 FP Notebook

90. Differences in Initial Hemodialysis Vascular Access Use Among Glomerulonephritis Subtypes in the United States. (PubMed)

Differences in Initial Hemodialysis Vascular Access Use Among Glomerulonephritis Subtypes in the United States. The type of vascular access used for hemodialysis affects patient morbidity and mortality. Whether vascular access types differ by glomerulonephritis (GN) subtype in the US hemodialysis population has not been investigated.Cross-sectional observational study.We identified all adult (aged ≥ 18 years) patients within the US Renal Data System who initiated hemodialysis therapy from July (...) % CI, 0.70-1.27] and 0.80 [95% CI, 0.56-1.13], respectively) but significantly less likely to have used an arteriovenous fistula (ORs of 0.66 [95% CI, 0.57-0.76] and 0.54 [95% CI, 0.45-0.63], respectively), whereas patients with any comparator primary GN subtype were at least as likely to have used either of these 2 access types.Potential misclassification of exposure; residual confounding by unmeasured covariates; inability to determine causes of observed associations; lacking longitudinal data

2016 American Journal of Kidney Diseases

91. The incidence, prevalence, and outcomes of glomerulonephritis derived from a large retrospective analysis. (PubMed)

The incidence, prevalence, and outcomes of glomerulonephritis derived from a large retrospective analysis. The incidence and period prevalence of glomerulonephritis (GN) with resultant rates of death and end-stage renal disease (ESRD) in the United States are unknown. Therefore, we assessed the presumptive burden of GN in a 20% Medicare sample, 5,442,495 individuals, and an Optum Clinformatics Employer Group Health Plan sample of 13,712,946 individuals. GN was established using International (...) Classification of Diseases, Ninth Revision, Clinical Modification claims-based algorithms. Outcomes were all-cause mortality and ESRD rates. Cox proportional hazards modeling was used to determine factors associated with outcomes in incident patients. For secondary (systemic immunologic disease) and primary GN, respectively, incidence rates per 100,000 patient-years were 134 (95% CI: 132-136) and 57 (56-58) in the Medicare cohort, and 10 (9-10) and 20 (19-21) in the health plan cohort. Period prevalence per

2016 Kidney International

92. CD4+ T Cell Fate in Glomerulonephritis: A Tale of Th1, Th17, and Novel Treg Subtypes (PubMed)

CD4+ T Cell Fate in Glomerulonephritis: A Tale of Th1, Th17, and Novel Treg Subtypes Multiple studies have identified CD4+ T cells as central players of glomerulonephritis (GN). Cells of the Th1 and Th17 responses cause renal tissue damage, while Tregs mediate protection. Recently, a high degree of plasticity among these T cell lineages was proposed. During inflammation, Th17 cells were shown to have the potential of transdifferentiation into Th1, Th2, or alternatively anti-inflammatory Tr1

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2016 Mediators of inflammation

93. Formation of tight junctions between neighboring podocytes is an early ultrastructural feature in experimental crescentic glomerulonephritis (PubMed)

Formation of tight junctions between neighboring podocytes is an early ultrastructural feature in experimental crescentic glomerulonephritis In crescentic glomerulonephritis (CGN), the development of cellular bridges between podocytes and parietal epithelial cells (PECs) triggers glomerular crescent formation. However, the sequential changes in glomerular ultrastructure in CGN are not well defined. This study investigated the time course of glomerular ultrastructure in experimental (...) . In vitro, the exposure of podocytes to macrophage-conditioned media altered cellular morphology and caused an intracellular redistribution of ZO-1.The formation of tight junctions between podocytes is an early ultrastructural abnormality in CGN, preceding FPE and podocyte bridge formation and occurring in response to inflammatory injury. Podocyte-to-podocyte tight junction formation may be a compensatory mechanism to maintain the integrity of the glomerular filtration barrier following severe

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2016 International journal of nephrology and renovascular disease

94. Crescentic Glomerulonephritis Associated with Pulmonary Tuberculosis (PubMed)

Crescentic Glomerulonephritis Associated with Pulmonary Tuberculosis Tuberculosis of kidney and urinary tract is caused by members of the Mycobacterium tuberculosis complex. Kidney is usually infected by haematogenous spread of bacilli from focus of infection in the lungs. Glomerular involvement in tuberculosis presenting as a rapidly progressive glomerulonephritis is a rare entity. We report a rare case of crescentic glomerulonephritis associated with pulmonary tuberculosis in a 26-year-old

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2016 Journal of clinical and diagnostic research : JCDR

95. Classifying murine glomerulonephritis using optical coherence tomography and optical coherence elastography (PubMed)

Classifying murine glomerulonephritis using optical coherence tomography and optical coherence elastography Acute glomerulonephritis caused by antiglomerular basement membrane marked by high mortality. The primary reason for this is delayed diagnosis via blood examination, urine analysis, tissue biopsy, or ultrasound and X-ray computed tomography imaging. Blood, urine, and tissue-based diagnoses can be time consuming, while ultrasound and CT imaging have relatively low spatial resolution (...) /OCE method could potentially be used as a minimally invasive tool for longitudinal studies during the progression and therapy of glomerulonephritis as well as complement and, perhaps, substitute highly invasive tissue biopsies. Elastic-wave propagation in mouse healthy and nephritic kidneys.© 2016 WILEY-VCH Verlag GmbH & Co. KGaA, Weinheim.

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2016 Journal of biophotonics

96. Reclassification of membranoproliferative glomerulonephritis: Identification of a new GN: C3GN (PubMed)

Reclassification of membranoproliferative glomerulonephritis: Identification of a new GN: C3GN This review revises the reclassification of the membranoproliferative glomerulonephritis (MPGN) after the consensus conference that by 2015 reclassified all the glomerulonephritis basing on etiology and pathogenesis, instead of the histomorphological aspects. After reclassification, two types of MPGN are to date recognized: The immunocomplexes mediated MPGN and the complement mediated MPGN. The latter (...) type is more extensively described in the review either because several of these entities are completely new or because the improved knowledge of the complement cascade allowed for new diagnostic and therapeutic approaches. Overall the complement mediated MPGN are related to acquired or genetic cause. The presence of circulating auto antibodies is the principal acquired cause. Genetic wide association studies and family studies allowed to recognize genetic mutations of different types as causes

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2016 World journal of nephrology

97. HBV-Associated Postinfectious Acute Glomerulonephritis: A Report of 10 Cases (PubMed)

HBV-Associated Postinfectious Acute Glomerulonephritis: A Report of 10 Cases Postinfectious acute glomerulonephritis (PIGN) may occur after various bacterial and viral infections. Hepatitis B virus (HBV) infection is a cause of chronic glomerulonephritis. We report here 10 cases (ages 7-20 years-old) of chronic HBV carriers with acute glomerulonephritis, with positive glomerular staining of hepatitis B surface antigen, and detectable presence of HBV DNA in the glomeruli. This form of PIGN, HBV (...) with non-HBV PIGN had complete or partial recovery. Pathologically, both HBV associated PIGN and non-HBV PIGN showed typical diffuse glomerular endocapillary proliferation, but HBV associated PIGN differed from classical PIGN with much fewer sub-epithelial glomerular "hump-shape" immune complex depositions. In conclusion, we have identified a novel association of HBV infection with acute glomerulonephritis.

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2016 PloS one

98. Clinical, Pathological, and Prognostic Characteristics of Glomerulonephritis Related to Staphylococcal Infection. (PubMed)

Clinical, Pathological, and Prognostic Characteristics of Glomerulonephritis Related to Staphylococcal Infection. Staphylococcal infection has become a common cause of postinfectious glomerulonephritis in the past 3 decades. Because few investigations focus on this disease, the demographics and clinicopathological features of glomerulonephritis related to staphylococcal infection are not well characterized. We conducted a pooled analysis of published literature in electronic databases (...) and analyzed the clinical features, laboratory findings, and histopathological changes. The patients were divided into 4 groups based on their prognosis: remission, persistent renal dysfunction, end-stage renal disease (ESRD), or death. A logistic regression model was used to identify the determinants of disease outcome. A total of 83 (64 men) patients with glomerulonephritis related to staphylococcal infection from 31 reports were analyzed. The mean age was 58 years (58 ± 17). Majority of the reports

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2016 Medicine

99. Rapidly progressive glomerulonephritis due to coexistent anti-glomerular basement membrane disease and fibrillary glomerulonephritis (PubMed)

Rapidly progressive glomerulonephritis due to coexistent anti-glomerular basement membrane disease and fibrillary glomerulonephritis Anti-glomerular basement membrane (anti-GBM) disease is a major cause of rapidly progressive glomerulonephritis (RPGN). On the other hand, fibrillary glomerulonephritis (GN) typically presents as proteinuria, hematuria and renal insufficiency, but rarely as RPGN. Without electron microscopy, the diagnosis of fibrillary GN can be missed. We report a 68-year-old

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2015 Clinical kidney journal

100. Fibrillary glomerulonephritis: presenting as crescentic glomerulonephritis causing rapidly progressive renal failure (PubMed)

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.

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2011 NDT Plus

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