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Glomerulonephritis Causes

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101. IgG4: a tantalizing link between causes of membranous glomerulonephritis and systemic disease. (Full text)

IgG4: a tantalizing link between causes of membranous glomerulonephritis and systemic disease. Alexander et al. give a detailed description of IgG4-related membranous glomerulonephritis (MGN). Their data delineate for the first time in IgG4-related disease (IgG4-RD) a second pattern of tissue injury occurring within the same organ. The paper highlights that MGN can occur alone or simultaneously with IgG4-related tubulointerstitial nephritis. Thus, it extends our understanding of IgG4-RD

2013 Kidney International PubMed

102. Proliferative glomerulonephritis causing acute renal failure in a child with Salmonella septicemia (Full text)

Proliferative glomerulonephritis causing acute renal failure in a child with Salmonella septicemia 23814433 2013 07 02 2018 11 13 0971-4065 23 3 2013 May Indian journal of nephrology Indian J Nephrol Proliferative glomerulonephritis causing acute renal failure in a child with Salmonella septicemia. 240-1 10.4103/0971-4065.111875 Dhooria G S GS Department of Pediatrics, Dayanand Medical College and Hospital, Ludhiana, India. Bains H S HS Bhat D D eng Journal Article India Indian J Nephrol

2013 Indian Journal of Nephrology PubMed

103. Kidney Transplant Recipients With Primary Membranous Glomerulonephritis Have a Higher Risk of Acute Rejection Compared With Other Primary Glomerulonephritides (Full text)

Kidney Transplant Recipients With Primary Membranous Glomerulonephritis Have a Higher Risk of Acute Rejection Compared With Other Primary Glomerulonephritides Despite being the leading cause of graft failure, there is a lack of published data about the rates of rejection in kidney transplant patients with glomerulonephritis as the cause of end-stage renal disease.We examined all consecutive adult (>18 years) renal transplant recipients with biopsy-proven native renal glomerular disease who (...) underwent kidney transplant between 1994 and 2013. Glomerulonephritis groups included were IgA nephropathy (IgAN) (N = 306), focal segmental glomerulosclerosis (FSGS) (N = 298), membranous nephropathy (MN) (N = 81), and lupus nephritis (LN) (N = 177).In the total cohort of 862 patients, 363 patients had an episode of acute rejection during the follow-up period of 19 years (incidence rate of 7.2% per year). Forty-five of 81 patients with MN had an episode of acute rejection during the follow-up period

2017 Transplantation direct PubMed

104. 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. (PubMed)

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

105. Discontinuation of antiretroviral therapy causing progression to end-stage renal disease in an HIV patient diagnosed with immune complex ‘lupus-like’ glomerulonephritis (Full text)

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 PubMed

106. Combination of Factor H Mutation and Properdin Deficiency Causes Severe C3 Glomerulonephritis. (Full text)

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 PubMed

107. 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

108. Lupus-like autoimmune disease caused by a lack of Xkr8, a caspase-dependent phospholipid scramblase (Full text)

Lupus-like autoimmune disease caused by a lack of Xkr8, a caspase-dependent phospholipid scramblase Apoptotic cells expose phosphatidylserine (PtdSer) on their cell surface and are recognized by macrophages for clearance. Xkr8 is a scramblase that exposes PtdSer in a caspase-dependent manner. Here, we found that among the three Xkr members with caspase-dependent scramblase activity, mouse hematopoietic cells express only Xkr8. The PtdSer exposure of apoptotic thymocytes, splenocytes (...) in the spleen of Xkr8-null mice, especially after the treatment with granulocyte colony-stimulating factor. Xkr8-null mice on an MRL background showed high levels of autoantibodies, splenomegaly with high levels of effector CD4 T cells, and glomerulonephritis development with immune-complex deposition at glomeruli. These results indicate that the Xkr8-mediated PtdSer exposure in apoptotic lymphocytes and aged neutrophils is essential for their clearance, and its defect activates the immune system, leading

2018 Proceedings of the National Academy of Sciences of the United States of America PubMed

109. Patients affected by a new variant of endemic pemphigus foliaceus have autoantibodies colocalizing with MYZAP, p0071, desmoplakins 1-2 and ARVCF, causing renal damage. (PubMed)

Patients affected by a new variant of endemic pemphigus foliaceus have autoantibodies colocalizing with MYZAP, p0071, desmoplakins 1-2 and ARVCF, causing renal damage. We have previously reported that about 30% of patients affected by a new variant of endemic pemphigus foliaceus (EPF) in El Bagre, Colombia (termed El Bagre-EPF or pemphigus Abreu-Manu) have systemic compromise. In the current study, we focused on studying autoreactivity to the kidney and its pathological correlations.To (...) , and additional interposition of membranoproliferative glomerulonephritis.© 2018 British Association of Dermatologists.

2018 Clinical & Experimental Dermatology

110. Focal mesangial proliferative glomerulonephritis in the rat caused by habu snake venom. A morphologic study. (Full text)

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 PubMed

111. Focal mesangial proliferative glomerulonephritis in the rat caused by Habu snake venom: the role of platelets. (Full text)

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 PubMed

112. New Streptococcal Serotypes Causing Pyoderma and Acute Glomerulonephritis Types 59, 60, and 61 (Full text)

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 PubMed

113. Hepatitis E Virus-Induced Cryoglobulinemic Glomerulonephritis in a Nonimmunocompromised Person. (PubMed)

Hepatitis E Virus-Induced Cryoglobulinemic Glomerulonephritis in a Nonimmunocompromised Person. Hepatitis E virus (HEV)-related kidney disease and symptomatic cryoglobulinemia have been observed in solid-organ transplant recipients. However, HEV RNA in the cryoprecipitate has not yet been assessed. We report what to our knowledge is the first documented case of autochthonous HEV-induced cryoglobulinemic crescentic and membranoproliferative glomerulonephritis in an immunocompetent man (...) with no notable medical history. He presented with edema, hypertension, increased serum creatinine level, and nephrotic syndrome. Type II cryoglobulinemia with monoclonal immunoglobulin G (IgG) κ light chain was detected. Anti-HEV IgG and IgM, as well as HEV RNA, were detected in serum and cryoprecipitate. Histologic analysis of a kidney biopsy specimen revealed features of crescentic and membranoproliferative glomerulonephritis. After HEV clearance, kidney and liver parameters improved and HEV RNA

2015 American Journal of Kidney Diseases

114. A case of membranoproliferative glomerulonephritis associated withcurved fibril deposition. (Full text)

A case of membranoproliferative glomerulonephritis associated withcurved fibril deposition. It is sometimes challenging to diagnose unsusual cases of fibrillary glomerulonephritis (FGN) and immunotactoid glomerulopathy (ITG), the rare causes of nephrotic syndrome.A 75-year-old Japanese woman presented with nephrotic syndrome, microhematuria and renal insufficiency. Renal biopsy revealed membranoproliferative glomerulonephritis (MPGN) with IgM and weak C3 deposition. Congo red stain was negative

2015 BMC Nephrology PubMed

115. A new rescue regimen with plasma exchange and rituximab in high-risk membranous glomerulonephritis. (PubMed)

A new rescue regimen with plasma exchange and rituximab in high-risk membranous glomerulonephritis. Even though current treatment guidelines for idiopathic membranous glomerulonephritis (iMGN) exist, many questions regarding an optimal therapy remain unanswered. Complete remission cannot be achieved in all patients; relapses occur, in some cases frequently, and side effects from the immunosuppressive therapy are common. Therapeutic options in high-risk patients not responding to standard (...) immunosuppressive therapies are limited. Recent research reveals that the human M-type phospholipase A2 receptor (PLA2 R) is a causative factor in iMGN that parallels clinical disease activity. However, in some patients, this correlation is not evident and additional undetermined factors seem to play a role.We evaluated a new rescue protocol including plasma exchanges (PE) against albumin, intravenous immunoglobulins (IVIGs) and rituximab for 10 patients with a biopsy-proven diagnosis of iMGN who were therapy

2015 European journal of clinical investigation

116. End-Stage Kidney Disease Due to Fibrillary Glomerulonephritis and Immunotactoid Glomerulopathy - Outcomes in 66 Consecutive ANZDATA Registry Cases. (PubMed)

End-Stage Kidney Disease Due to Fibrillary Glomerulonephritis and Immunotactoid Glomerulopathy - Outcomes in 66 Consecutive ANZDATA Registry Cases. Fibrillary glomerulonephritis (FGN) and immunotactoid glomerulopathy (IG) are uncommon and characterised by non-amyloid fibrillary glomerular deposits. The aim of this study was to investigate characteristics and outcomes of patients undergoing renal replacement therapy (RRT) for end-stage kidney disease (ESKD) secondary to FGN and IG.All ESKD (...) patients who commenced RRT in Australia and New Zealand 1 January 1990 to 31 December 2010 were included. Outcomes were assessed by Kaplan-Meier, multivariate logistic-regression analysis and multivariable Cox proportional-hazards survival analysis.Of 45,216 individuals with ESKD, 55 (0.12%) had FGN and 11 (0.02%) had IG. The median survival of FGN patients on dialysis (5.63 years, 95% CI 3.31-7.96) was not significantly different from patients with other ESKD causes (median 4.01 years, 95% CI 4.34

2015 American journal of nephrology

117. The Prevalence and Management of Pauci-Immune Glomerulonephritis and Vasculitis in Western Countries (Full text)

The Prevalence and Management of Pauci-Immune Glomerulonephritis and Vasculitis in Western Countries Pauci-immune glomerulonephritis is the most common cause of aggressive glomerulonephritis and occurs as a renal-limited disease or as a component of systemic necrotizing small-vessel vasculitis. It is characterized by paucity of staining for immunoglobulins, by immunofluorescence along with fibrinoid necrosis and crescent formation by light microscopy, while the vast majority of patients have (...) anti-neutrophil cytoplasmic antibodies (ANCA) in their circulation, which also participate in the pathogenesis of the disease.Pauci-immune glomerulonephritis often manifests with rapidly deteriorating kidney function, which may be accompanied by distinctive clinical features of systemic necrotizing small-vessel vasculitis of one the following clinical phenotypes: microscopic polyangiitis, granulomatosis with polyangiitis or eosinophilic granulomatosis with polyangiitis. These are associated

2015 Kidney Diseases PubMed

118. Necrotizing and crescentic glomerulonephritis with membranous nephropathy in a patient exposed to levamisole-adulterated cocaine (Full text)

Necrotizing and crescentic glomerulonephritis with membranous nephropathy in a patient exposed to levamisole-adulterated cocaine Levamisole is an antihelminthic agent widely used as an adulterant of illicit cocaine recently implicated as a cause of antineutrophil cytoplasmic antibody (ANCA)-associated microscopic polyangiitis in cocaine abusers. An isolated case of membranous nephropathy (MN) associated with levamisole exposure has also been reported. We report the first case, to our knowledge (...) , of a patient with both microscopic polyangiitis manifest as a pauci-immune necrotizing and crescentic glomerulonephritis and concurrent MN in the setting of chronic cocaine abuse and presumed levamisole exposure, raising the hypothesis that levamisole was the causative agent in the development of this rare dual glomerulopathy.

2015 Clinical kidney journal PubMed

119. Hypertension in Chronic Glomerulonephritis (Full text)

Hypertension in Chronic Glomerulonephritis Chronic glomerulonephritis (GN), which includes focal segmental glomerulosclerosis and proliferative forms of GN such as IgA nephropathy, increases the risk of hypertension. Hypertension in chronic GN is primarily volume dependent, and this increase in blood volume is not related to the deterioration of renal function. Patients with chronic GN become salt sensitive as renal damage including arteriolosclerosis progresses and the consequent renal (...) ischemia causes the stimulation of the intrarenal renin-angiotensin-aldosterone system(RAAS). Overactivity of the sympathetic nervous system also contributes to hypertension in chronic GN. According to the KDIGO guideline, the available evidence indicates that the target BP should be ≤140mmHg systolic and ≤90mmHg diastolic in chronic kidney disease patients without albuminuria. In most patients with an albumin excretion rate of ≥30mg/24 h (i.e., those with both micro-and macroalbuminuria), a lower

2015 Electrolytes & Blood Pressure : E & BP PubMed

120. Suppression of Rapidly Progressive Mouse Glomerulonephritis with the Non-Steroidal Mineralocorticoid Receptor Antagonist BR-4628 (Full text)

(collagen I, fibronectin). In addition, treatment with BR-4626 did not cause hyperkalaemia or increase urine Na+/K+ excretion (a marker of tubular dysfunction).The non-steroidal MRA (BR-4628) provided substantial suppression of mouse crescentic glomerulonephritis without causing tubular dysfunction. This finding warrants further investigation of non-steroidal MRAs as a therapy for inflammatory kidney diseases. (...) Suppression of Rapidly Progressive Mouse Glomerulonephritis with the Non-Steroidal Mineralocorticoid Receptor Antagonist BR-4628 Steroidal mineralocorticoid receptor antagonists (MRAs) are effective in the treatment of kidney disease; however, the side effect of hyperkalaemia, particularly in the context of renal impairment, is a major limitation to their clinical use. Recently developed non-steroidal MRAs have distinct characteristics suggesting that they may be superior to steroidal MRAs

2015 PloS one PubMed

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