View clinical trials related to Glomerulonephritis.
Filter by:Focal segmental glomerulosclerosis (FSGS) is one of the most common primary glomerular diseases leading to end stage renal disease. In this study, our aim is to evaluate the effects of histopathological, clinical, and laboratory features of patients with primary FSGS on the disease progression.
The primary objective of this study was to determine whether ACH-0144471 (also known as danicopan and ALXN2040) increases blood C3 complement protein (C3) levels in participants with low C3 levels due to either C3G or IC-MPGN.
This study is being done to see if daratumumab is safe and effective in the treatment of proliferative glomerulonephritis with monoclonal immune deposits (PGNMID) and C3 glomerulopathy associated with monoclonal gammopathy (C3GN). This is an inflammatory disease in the kidney due to the production of abnormal proteins. There are no known standard effective treatments for patients with PGNMID and C3GN secondary to monoclonal gammopathy. These diseases are caused by abnormal production of proteins (monoclonals) by abnormal clones. Daratumamb has been shown to be effective in treating patients with multiple myeloma a disease which also caused by over production of monoclonal proteins from abnormal clones. Everyone in this study will receive daratumumab.
Anti-glomerular basement membrane (GBM) glomerulonephritis is a rare autoimmune disease mediated by anti-GBM antibodies and characterized by acute renal failure due to diffuse crescentic glomerulonephritis. Established treatment is cyclophosphamide and corticosteroids to suppress anti-GBM production and daily plasma exchange to remove circulating anti-GBM antibodies. The vast majority of patients with anti-GBM glomerulonephritis develop irreversible end-stage renal failure despite this treatment. Immunoadsorption may lower anti-GBM titres more effectively than plasma exchange. The goal of this interventional open, non-randomized pilot study is to study the efficacy, adverse events, logistic feasibility and costs of immuno-adsorption for the removal of anti-GBM antibodies in patients with acute renal failure due to anti-GBM glomerulonephritis. Eight patients with acute renal failure due to anti-GBM glomerulonephritis with or without accompanying pulmonary involvement will be treated with daily immunoadsorption, instead of plasma exchange, until anti-GBM titres are undetectable. All other aspects of the treatment (e.g. immunosuppressive treatment, renal replacement therapy) will be standard. The primary study parameter is the number of days that anti-GBM antibody titre is above a toxic level, defined as >30 ELISA units. Secondary study parameters are the tolerability and adverse events of immunoadsorption, the logistic feasibility defined as the time interval between diagnosis and start of first immunoadsorption treatment and costs of immunoadsorption.
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.
The estimation of the cardiovascular risk in the general population must take into account small renal disturbances, as the microalbuminuria. Conversely certain parameters of the cardiovascular risk influence the evolution of renal diseases, for example the arterial high blood pressure. The measure of the activity of the autonomous nervous system, and especially the quantification of its variability, is a means to estimate the cardiovascular risk. The investigators formulate the hypothesis that the variability of the autonomous nervous system is an additional clinical element for the evaluation of the evolutionary risk of renal diseases. The aim of this study is to compare the variability of the autonomous nervous system during the various evolutionary stages of the renal disease. The renal disease studied will be IgA nephropathy (IgNA). IgNA is a histologically defined glomerulonephritis (rela biopsy) by the presence of deposits immunoglobulin A (IgA) in the renal mesangium (at list 1+) by immunofluorescence.
The investigators hypothesize that using Losartan would help decrease proteinuria in controlling proteinuria in children with immunoglobulin A nephropathy.
This pilot study is being done to see if the study medication, Rituximab, preserves kidney function after 12 months of taking the drug.
Membranoproliferative glomerulonephritis (MPGN) is the third or fourth leading cause of end stage renal disease among the primary glomerulonephritis. Hyperactivation of the alternative complement pathway and familial forms for all types of MPGN have been reported suggesting that genetic abnormalities may play a predisposing role to the disease. In recent case reports Eculizumab, a monoclonal antibody that binds to C5 to prevent formation of the membrane attack complex ,is a safe and effective therapy.
This is a phase II, open label, experimental medicine study to evaluate the efficacy, safety and mechanism of action of belimumab in subjects with antiphospholipase A2 receptor (PLA2R) autoantibody positive idiopathic membranous glomerulonephropathy (IMGN), and to profile the relationship between biomarkers, autoantibody status and clinical response. 10 milligrams per kilogram (mg/kg) belimumab intravenous (IV) will be administered at weeks 0, 2, and then every 4 weeks, over a 24-week treatment period in subjects with anti-PLA2R antibody positive IMGN followed by a further long term treatment period until subjects reach remission of proteinuria, up to a maximum of 2 years total treatment. All subjects will receive background supportive therapy throughout the study. The dosing frequency will be adjusted to every 2 weeks if the subject's proteinuria as assessed by urinary protein creatinine ratio (PCR) is greater than 1000 milligrams per millimole (mg/mmol) [greater than 10 grams(g)/24 hours (h)], to compensate for loss of belimumab in the urine. Effects on mechanistic markers will be measured by the level of proteinuria, levels of anti-PLA2R antibodies, and various other measures of kidney function. These will be compared to historical data. The pharmacokinetics of belimumab will be measured to confirm dosing in heavily proteinuric subjects. Pharmacodynamic (PD) markers, biomarkers and Quality of Life(QoL) in IMGN subjects will also be investigated. Safety will be assessed by adverse events (AE), clinical laboratory evaluations, and vital signs.