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Glomerulonephritis Causes

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81. Glomerulonephritis Causes

Glomerulonephritis Causes Glomerulonephritis Causes 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 Glomerulonephritis Causes (...) Glomerulonephritis Causes Aka: Glomerulonephritis Causes , Infectious Causes of Glomerulonephritis From Related Chapters II. Causes: Primary Glomerular Disease IgA Nephropathy Mesangial proliferative disease Membranoproliferative disease Antiglomerular basement membrane III. Causes: Infectious l Acute bacteremia Pneumococcal bacteremia Visceral Viral A and B (EBV) Parasitic IV. Causes: Multisystem Disease Postpartum Hereditary nephritis Cryoglobulinemia V. Causes: Medications (primarily cause RPGN) See Examples

2015 FP Notebook

82. Discontinuation of antiretroviral therapy causing progression to end-stage renal disease in an HIV patient diagnosed with immune complex ‘lupus-like’ glomerulonephritis Full Text available with Trip Pro

Discontinuation of antiretroviral therapy causing progression to end-stage renal disease in an HIV patient diagnosed with immune complex ‘lupus-like’ glomerulonephritis Immune complex 'lupus-like glomerulonephritis' is a type of renal injury seen infrequently in human immunodeficiency virus (HIV) patients and very little is known about the clinical course and treatment. Treatment options are limited but antiretroviral therapy and steroids have been tried with limited success. We report (...) a case of a 21-year-old HIV-positive African American male with lupus-like glomerulonephritis who progressed to end-stage renal disease upon discontinuation of highly active antiretroviral therapy. This case illustrates the importance of antiretroviral therapy as an important treatment modality for immune complex lupus-like glomerulonephritis in HIV patients.

2012 Clinical kidney journal

83. Combination of Factor H Mutation and Properdin Deficiency Causes Severe C3 Glomerulonephritis. Full Text available with Trip Pro

Combination of Factor H Mutation and Properdin Deficiency Causes Severe C3 Glomerulonephritis. Factor H (fH) and properdin both modulate complement; however, fH inhibits activation, and properdin promotes activation of the alternative pathway of complement. Mutations in fH associate with several human kidney diseases, but whether inhibiting properdin would be beneficial in these diseases is unknown. Here, we found that either genetic or pharmacological blockade of properdin, which we expected

2012 Journal of the American Society of Nephrology

84. The IgG-degrading enzyme of Streptococcus pyogenes causes rapid clearance of anti-glomerular basement membrane antibodies in patients with refractory anti-glomerular basement membrane disease. Full Text available with Trip Pro

The IgG-degrading enzyme of Streptococcus pyogenes causes rapid clearance of anti-glomerular basement membrane antibodies in patients with refractory anti-glomerular basement membrane disease. In anti-glomerular basement membrane (anti-GBM) disease, IgG class autoantibodies induce rapidly progressive glomerulonephritis. Regrettably, many patients are diagnosed at a late stage when even intensive conventional treatment fails to restore renal function The endopeptidase IdeS (Immunoglobulin G (...) patients. After about a week, all rebounded but the rebounds were easily managed by plasma exchange in two of three cases. Renal histology demonstrated severe crescentic glomerulonephritis with acute but mainly chronic changes. Staining for the Fc fragment was negative in all while Fab was positive in two patients. Unfortunately, none of the patients regained independent renal function. Thus, treatment with IdeS led to rapid clearance of circulating and kidney bound anti-GBM antibodies. The clinical

2019 Kidney International

85. New Streptococcal Serotypes Causing Pyoderma and Acute Glomerulonephritis Types 59, 60, and 61 Full Text available with Trip Pro

New Streptococcal Serotypes Causing Pyoderma and Acute Glomerulonephritis Types 59, 60, and 61 Three new streptococcal M serotypes, types 59, 60, and 61; have been described. They were first isolated from patients with pyoderma and acute glomerulonephritis (AGN), seen during epidemiological studies in Alabama. A possible antigenic relationship between types 59 and 61 was suggested by their T-agglutination reactions; a more specific T antiserum prepared for type 59 was useful in separating

1974 Infection and immunity

86. Focal mesangial proliferative glomerulonephritis in the rat caused by habu snake venom. A morphologic study. Full Text available with Trip Pro

Focal mesangial proliferative glomerulonephritis in the rat caused by habu snake venom. A morphologic study. A new model of focal mesangial proliferative glomerulonephritis in the rat has been produced by intravenous habu snake venom. Glomerulonephritis developed in 70% of rats surviving the first 6 hours after venom administration. The earliest ultrastructural change (10 minutes after venom) was the presence of loose platelet aggregates and free granules in the capillary lumen and mesangium

1977 The American journal of pathology

87. Focal mesangial proliferative glomerulonephritis in the rat caused by Habu snake venom: the role of platelets. Full Text available with Trip Pro

Focal mesangial proliferative glomerulonephritis in the rat caused by Habu snake venom: the role of platelets. Platelet aggregates are a prominent early feature in the glomerular lesions of focal mesangial proliferative glomerulonephritis induced by Habu venom. After venom injection the peripheral blood platelet count falls rapidly, and in vitro the venom causes platelet aggregation and release of 5-HT. The role of platelets in this model has been studied in rats depleted of platelets

1979 British journal of experimental pathology

88. Simultaneous comprehensive multiplex autoantibody analysis for rapidly progressive glomerulonephritis. Full Text available with Trip Pro

Simultaneous comprehensive multiplex autoantibody analysis for rapidly progressive glomerulonephritis. Rapidly progressive glomerulonephritis (RPGN) is mainly caused by anti-glomerular basement membrane (GBM) antibody-mediated glomerulonephritis, immune-complex or anti-neutrophil cytoplasmic antibody (ANCA)-associated vasculitides and leads to rapid loss of renal function. Detection of ANCA and autoantibodies (autoAbs) to GBM and dsDNA enables early diagnosis and appropriate treatment of RPGN

2016 Medicine

89. Recent advances in our understanding of recurrent primary glomerulonephritis after kidney transplantation. (Abstract)

Recent advances in our understanding of recurrent primary glomerulonephritis after kidney transplantation. Recurrent glomerulonephritis (GN) is an important cause of kidney allograft failure, particularly in younger recipients. Approximately 15% of death-censored graft failures are due to recurrent GN, but this incidence is likely an underestimation of the magnitude of the problem. Overall, 18% to 22% of kidney allografts are lost due to GN, either recurrent or presumed de novo. The impact (...) on the most common forms of primary GN, including focal segmental glomerulosclerosis, membranous nephropathy, membranoproliferative glomerulonephritis, and IgA nephropathy. New understanding of the pathogenesis of these diseases has had direct clinical implications for transplantation, allowing better identification of candidates at high risk of recurrence and earlier diagnoses, and it is expected to lead to significance improvements in the therapy and perhaps even prevention of GN recurrence. More than

2016 Kidney International

90. Clinical, Pathological, and Prognostic Characteristics of Glomerulonephritis Related to Staphylococcal Infection. Full Text available with Trip Pro

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

2016 Medicine

91. Manifestations of Complement-Mediated and Immune Complex-Mediated Membranoproliferative Glomerulonephritis: A Comparative Consecutive Series. (Abstract)

Manifestations of Complement-Mediated and Immune Complex-Mediated Membranoproliferative Glomerulonephritis: A Comparative Consecutive Series. Membranoproliferative glomerulonephritis (MPGN) recently was reclassified to reflect the underlying cause as a complement-mediated and immune complex-mediated disease. This classification is based on renal biopsy immunofluorescence examination, making the former electron-microscopy classification obsolete. In this report, we describe related eye findings

2016 Ophthalmology

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

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

93. Pauci Immune crescentic glomerulonephritis in a patient with T-cell lymphoma and argyria. Full Text available with Trip Pro

Pauci Immune crescentic glomerulonephritis in a patient with T-cell lymphoma and argyria. Silver is a transition metal, toxic when ingested in significant amounts, causing argyria (skin deposition) and argyrosis (eye deposition). It is excreted mainly via the gastrointestinal tract with only small amounts eliminated by the kidneys, and rarely have cases of nephrotoxicity due to silver been reported. Here we present the case of a woman who used colloidal silver as an alternative remedy for a T (...) cell lymphoma, who subsequently developed argyria and a pauci-immune crescentic glomerulonephritis with evidence of extensive glomerular basement membrane silver deposition.A 47 year old woman of Indo-Asian descent with a T-cell lymphoma who refused conventional chemotherapy for 18 months but self-medicated with a remedy containing colloidal silver, was admitted with acute dialysis-dependent kidney injury. A kidney biopsy demonstrated a pauci-immune crescentic glomerulonephritis with deposition

2016 BMC Nephrology

94. Innate and adaptive immunity in experimental glomerulonephritis: a pathfinder tale. Full Text available with Trip Pro

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.

2016 Pediatric Nephrology

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

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

96. Small vessel microembolization and acute glomerulonephritis following infection of aesthetic filler implants Full Text available with Trip Pro

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.

2016 Diagnostic pathology

97. Crescentic Glomerulonephritis Associated with Pulmonary Tuberculosis Full Text available with Trip Pro

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

2016 Journal of clinical and diagnostic research : JCDR

98. ANCA-negative eosinophilic granulomatosis with polyangitis (EGPA) manifesting as a large intracardiac thrombus and glomerulonephritis with angionecrosis Full Text available with Trip Pro

ANCA-negative eosinophilic granulomatosis with polyangitis (EGPA) manifesting as a large intracardiac thrombus and glomerulonephritis with angionecrosis A 59-year-old woman with a history of bronchial asthma presented with a prolonged fever and eosinophilia. There was transient proteinuria and troponin level was elevated. Antineutrophil cytoplasmic antibody was negative and she did not fulfil criteria for eosinophilic granulomatosis with polyangitis (EGPA). Echocardiography showed a large (...) as a rare presenting sign for EGPA and underscores current complicated strategy to diagnose EGPA. Of note, this clinical challenge was mostly caused by inchoate comprehension of hypereosinophilia-related disorders. 2016 BMJ Publishing Group Ltd.

2016 BMJ case reports

99. Reclassification of membranoproliferative glomerulonephritis: Identification of a new GN: C3GN Full Text available with Trip Pro

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

2016 World journal of nephrology

100. Classifying murine glomerulonephritis using optical coherence tomography and optical coherence elastography Full Text available with Trip Pro

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.

2016 Journal of biophotonics

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