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Glomerulonephritis Causes

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101. Extreme Thrombocytosis Presenting in Anti-Neutrophil Cytoplasmic Autoantibodies-Associated Crescentic Glomerulonephritis with Immune Complex Deposits: A Case Report Full Text available with Trip Pro

Extreme Thrombocytosis Presenting in Anti-Neutrophil Cytoplasmic Autoantibodies-Associated Crescentic Glomerulonephritis with Immune Complex Deposits: A Case Report We describe a female patient with extreme reactive thrombocytosis (RT) in anti-neutrophil cytoplasmic autoantibodies (ANCA)-associated crescentic glomerulonephritis (CGN) with immune complex deposits, which has never been reported before.A female adolescent with symptoms of oliguria and gross hematuresis had serious renal function (...) cause a severe inflammatory state, leading to extreme RT. The roles that the immune complex and ANCA play on the effect of the platelet count and function in CGN need further research.

2016 Iranian Red Crescent medical journal

102. Bartonella Endocarditis and Pauci-Immune Glomerulonephritis: A Case Report and Review of the Literature Full Text available with Trip Pro

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

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

103. HBV-Associated Postinfectious Acute Glomerulonephritis: A Report of 10 Cases Full Text available with Trip Pro

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.

2016 PloS one

104. Formation of tight junctions between neighboring podocytes is an early ultrastructural feature in experimental crescentic glomerulonephritis Full Text available with Trip Pro

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

2016 International journal of nephrology and renovascular disease

105. CD4+ T Cell Fate in Glomerulonephritis: A Tale of Th1, Th17, and Novel Treg Subtypes Full Text available with Trip Pro

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

2016 Mediators of inflammation

106. Anti-glomerular basement membrane crescentic glomerulonephritis: A report from India and review of literature Full Text available with Trip Pro

Anti-glomerular basement membrane crescentic glomerulonephritis: A report from India and review of literature Anti-glomerular basement membrane (anti-GBM) disease is an autoimmune disease that most commonly presents as rapidly progressive glomerulonephritis with or without pulmonary involvement. It is characterized by the presence of antibodies directed to antigenic targets within glomerular and alveolar basement membranes. This study was performed to evaluate the clinicopathological features (...) and outcome in anti-GBM crescentic glomerulonephritis (CrGN) at a tertiary care center in North India over a period of 9 years (January 2004 to December 2012). A diagnosis of anti-GBM CrGN was made in the presence of >50% crescents, linear deposits of IgG along GBM, and raised serum anti-GBM antibody titer. Of 215 cases of CrGN diagnosed during this period, 11 had anti-GBM CrGN. Anti-GBM CrGN was found at all ages but was most common in the third to fifth decade with no gender predilection (mean age 48

2016 Indian Journal of Nephrology

107. C3 mesangial proliferative glomerulonephritis initially presenting with atypical hemolytic uremic syndrome: a case report Full Text available with Trip Pro

C3 mesangial proliferative glomerulonephritis initially presenting with atypical hemolytic uremic syndrome: a case report Hemolytic uremic syndrome is characterized by acute renal failure, thrombocytopenia, and Coombs-negative hemolytic anemia. In C3 mesangial proliferative glomerulonephritis, an increase in mesangial cell proliferation without thickening in the glomerular capillary wall can be seen under light microscopy, but the definitive diagnosis is made with the immunohistologic (...) demonstration of isolated C3 deposits in the mesangium. C3 glomerulonephritis may be detected in childhood; however, in this case report we describe the first case of isolated C3 glomerulonephritis together with atypical hemolytic uremic syndrome in an adult patient.Here we present a case of a 27-year-old white man with anuria who was hospitalized after being diagnosed as having hemolytic uremic syndrome accompanied by acute renal failure. Renal biopsy results revealed C3 glomerulonephritis

2016 Journal of medical case reports

108. Recurrent Glomerulonephritis After Renal Transplantation

Go to Brief Summary: Glomerulonephritis (GN) is the leading cause of end-stage renal disease in 30% to 50% of patients who receive a renal transplant. The exact prevalence of either recurrent or de novo GN is unknown since a considerable number of patients never undergo allograft biopsy, leaving GN underdiagnosed. The aim of this study is to evaluate the effects of recurrent GN on the prevalence, risk factors, clinicopathological features, and outcome of renal transplant recipients. Condition (...) or disease Glomerulonephritis Detailed Description: Glomerulonephritis is the leading cause of end-stage renal disease in 30% to 50% of patients who receive a renal transplant. Even though recurrent or de novo posttransplant primary GN is the third most frequent cause of renal allograft loss after renal transplantation, different recurrence rates have been reported in different patient series worldwide. With the implementation of diverse and improved immunosuppressive treatment regimens and prolongation

2016 Clinical Trials

109. Nivolumab-associated acute glomerulonephritis: a case report and literature review. Full Text available with Trip Pro

, the patient's kidney function improved to his baseline level. Despite a prolonged interruption to treatment, immunosuppressive therapy did not compromise the anticancer effects of nivolumab.Immune-related adverse effects in the kidney can cause autoimmune glomerulonephritis as well as tubulointerstitial injury. In the literature, immune-related nephritis generally responded well to systemic corticosteroid treatment. Based on our experience, a prolonged course of a high dose of steroids and hemodialysis may (...) Nivolumab-associated acute glomerulonephritis: a case report and literature review. Immune checkpoint inhibitors are changing the landscape of oncology treatment as they are significantly improving treatment for multiple malignancies. Nivolumab, an anti-programmed death 1 antibody, is a US Food and Drug Administration-approved treatment for melanoma, non-small cell lung cancer, and kidney cancer but can result in a spectrum of autoimmune side effects. Adverse effects can occur within any organ

2016 BMC Nephrology

110. The Prevalence and Management of Pauci-Immune Glomerulonephritis and Vasculitis in Western Countries Full Text available with Trip Pro

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

111. Hepatitis E Virus-Induced Cryoglobulinemic Glomerulonephritis in a Nonimmunocompromised Person. (Abstract)

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

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

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

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

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

114. A case of membranoproliferative glomerulonephritis associated withcurved fibril deposition. Full Text available with Trip Pro

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

115. Necrotizing ANCA-Positive Glomerulonephritis Secondary to Culture-Negative Endocarditis Full Text available with Trip Pro

Necrotizing ANCA-Positive Glomerulonephritis Secondary to Culture-Negative Endocarditis Infective endocarditis (IE) and small-vessel vasculitis may have similar clinical features, including glomerulonephritis. Furthermore the association between IE and ANCA positivity is well documented, making differential diagnosis between IE- and ANCA-associated vasculitis particularly difficult, especially in case of culture-negative IE. We report on one patient with glomerulonephritis secondary to culture (...) -negative IE caused by Bartonella henselae which illustrates this diagnostic difficulty.

2015 Case reports in nephrology

116. Hypertension in Chronic Glomerulonephritis Full Text available with Trip Pro

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

117. Necrotizing and crescentic glomerulonephritis with membranous nephropathy in a patient exposed to levamisole-adulterated cocaine Full Text available with Trip Pro

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

118. Suppression of Rapidly Progressive Mouse Glomerulonephritis with the Non-Steroidal Mineralocorticoid Receptor Antagonist BR-4628 Full Text available with Trip Pro

(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

119. Sjögren Syndrome and Cryoglobulinemic Glomerulonephritis. Full Text available with Trip Pro

wall staining was observed on immunofluorescence with antisera to C3 and immunoglobulin M (IgM), with less intense staining indicative of IgG and κ and λ light chains. A biopsy diagnosis of Sjögren syndrome-related cryoglobulinemic membranoproliferative glomerulonephritis and vasculitis was rendered. Subsequent investigations revealed the presence of circulating type II cryoglobulins with cryocrit of 9%. Although rare, Sjögren syndrome is the most common cause of non-hepatitis C virus-related mixed (...) Sjögren Syndrome and Cryoglobulinemic Glomerulonephritis. We report the case of a 53-year-old woman with Sjögren syndrome and cryoglobulinemia. The patient presented with nephrotic syndrome, hematuria, and reduced estimated glomerular filtration rate. The kidney biopsy revealed diffuse endocapillary proliferation and leukocyte exudation with focal intraluminal hyaline thrombi, prominent tubulointerstitial inflammation, and vasculitis. Diffuse granular mesangial and segmental to global capillary

2015 American Journal of Kidney Diseases

120. Renal participation of myeloperoxidase in antineutrophil cytoplasmic antibody (ANCA)-associated glomerulonephritis. Full Text available with Trip Pro

Renal participation of myeloperoxidase in antineutrophil cytoplasmic antibody (ANCA)-associated glomerulonephritis. Myeloperoxidase (MPO) is an important neutrophil lysosomal enzyme, a major autoantigen, and a potential mediator of tissue injury in MPO-ANCA-associated vasculitis (MPO-AAV) and glomerulonephritis. Here we examined MPO deposition in kidney biopsies from 47 patients with MPO-AAV. Leukocyte accumulation and fibrin deposition consistent with cell-mediated immunity was a major feature (...) ) correlated with intraglomerular CD4+ cells and MPO+ macrophages. Thus, cellular and extracellular MPO may cause glomerular and interstitial injury.

2015 Kidney International

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