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Glomerulonephritis clinical trials

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NCT ID: NCT01610492 Completed - Clinical trials for Glomerulonephritis, Membranous

A Study of Belimumab in Idiopathic Membranous Glomerulonephropathy

Start date: July 1, 2012
Phase: Phase 2
Study type: Interventional

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.

NCT ID: NCT01560052 Completed - Clinical trials for IgA Glomerulonephritis

Therapeutic Evaluation of Steroids in IgA Nephropathy Global Study (TESTING Low Dose Study)

TESTING
Start date: May 5, 2012
Phase: N/A
Study type: Interventional

This study will evaluate the long-term efficacy and safety of low dose oral methylprednisolone compared to matching placebo, on a background of routine RAS inhibitor therapy, in preventing kidney events in patients with IgA nephropathy and features suggesting a high risk of progression.

NCT ID: NCT01221181 Completed - Clinical trials for Dense Deposit Disease

Eculizumab Therapy for Dense Deposit Disease and C3 Nephropathy

Start date: July 2010
Phase: Phase 1
Study type: Interventional

This open label, non-blinded, proof of concept efficacy and safety study of eculizumab in patients with biopsy proven DDD or C3 nephropathy. The trial will consist of adult patients with these diseases who have > 1 gram of proteinuria or a decreased glomerular filtration rate (GFR), both predictors of a poor long-term outcome in many glomerular diseases. The patients will be treated with eculizumab for one year. The goals will be to determine whether treatment leads to an improvement in kidney function, defined by remissions of proteinuria and improvements in estimated GFR (measured by serum creatinine), and to improvement in histologic parameters, including percentage of non-affected glomeruli, interstitial fibrosis, intensity of C3 staining of immunofluorescence, and amount of electron dense deposits by electron microscopy.

NCT ID: NCT01115426 Completed - Clinical trials for IGA Glomerulonephritis

Inhibitors of Angiotensin II in Proteinuric Mesangioproliferative Glomerulonephritis

Start date: January 1997
Phase: Phase 4
Study type: Interventional

This study evaluates prospectively the effects of an anti-angiotensin II regimen on renal outcome in patients with mesangioproliferative glomerulonephritis followed-up for 10 years.

NCT ID: NCT01093157 Completed - Glomerulonephritis Clinical Trials

A Dose Escalation Study of Long-acting ACTH Gel in Membranous Nephropathy

Start date: February 2010
Phase: Phase 1/Phase 2
Study type: Interventional

Membranous Nephropathy (MN) is an immune-mediated kidney disease that affects the glomerulus or the filter that removes toxins from the blood. Damage to the membrane that separates blood from urine results in loss of protein into the urine (proteinuria) and in some cases loss of kidney function.There is no standard specific treatment for MN. ACTH has a pronounced lipid-lowering effect in healthy individuals, in steroid-treated patients with renal disease and in hemodialysis patients Some studies suggest that prolonged synthetic ACTH therapy may represent an effective therapy in patients with idiopathic MN, more extensive randomized studies with longer follow-up are needed before therapeutic recommendations can be made. We propose to do a pilot study to test the hypothesis that biologic ACTH, a slow-release formulation of corticotropin extracted from porcine pituitary glands (H.P. Acthar gel) will be effective in reducing proteinuria and improving lipid profile in patients with idiopathic MN.

NCT ID: NCT00983034 Completed - Nephrotic Syndrome Clinical Trials

The Effects of Helicobacter Pylori Eradication on Proteinuria in Patients With Membranous Nephropathy

Start date: March 2006
Phase: N/A
Study type: Interventional

Membranous nephropathy (MN) may also be secondary to many other diseases (e.g., infections, drugs, neoplasms and autoimmune diseases). In this study, the presence of Helicobacter Pylori (H. pylori) antigen was investigated in renal tissue from needle biopsy samples, and the prevalence of H. pylori infection and the effects of H. pylori eradication on proteinuria level in patients with MN will be investigated.

NCT ID: NCT00914524 Completed - Clinical trials for Diabetic Nephropathy

Study of Olmesartan Medoxomil (CS-866) in Patients With Chronic Glomerulonephritis or Diabetic Nephropathy

Start date: January 2005
Phase: Phase 2
Study type: Interventional

The treatment period was 16 weeks, the initial dose, 5 mg, was unforcedly titrated to 10 mg, 20 mg and 40 mg after confirming tolerance at weeks 4, 8 and 12. The primary endpoint for efficacy was the change in the urinary protein/creatinine ratio from baseline to the end of treatment. The secondary endpoint was creatinine clearance (Ccr).

NCT ID: NCT00843856 Completed - Clinical trials for Glomerulonephritis, Membranous

Mycophenolate Mofetil and Tacrolimus Versus Tacrolimus for the Treatment of Idiopathic Membranous Glomerulonephritis

MTAC
Start date: March 3, 2009
Phase: Phase 4
Study type: Interventional

Study Hypothesis: When mycophenolate mofetil is added to tacrolimus in the treatment of membranous glomerulonephritis it is likely to improve the initial response to treatment and reduce the risk of relapse on stopping therapy.

NCT ID: NCT00818948 Completed - Clinical trials for Systemic Lupus Erythematosus

Safety Study of AMG 811 in Subjects With Systemic Lupus Erythematosus With and Without Glomerulonephritis

Start date: March 2009
Phase: Phase 1
Study type: Interventional

This is a 2-part, multi-center, randomized, double-blind, placebo-controlled, multiple dose escalation study, enrolling approximately 48 subjects. Part A of the study will enroll subjects with Systemic Lupus Erythematosus (SLE) without Glomerulonephritis (GN) into 3 cohorts. Part B of the study will enroll SLE subjects with GN into 3 cohorts. The purpose of the study is to evaluate the multiple dose of AMG 811 on safety. Tolerability and pharmacokinetics.

NCT ID: NCT00521508 Completed - Clinical trials for Glomerulonephritis, IGA

Role of Regulatory T Cells in Pathogenesis of Primary IgA Nephropathy

Start date: April 2008
Phase: N/A
Study type: Interventional

Along structural IgA abnormalities, hyperproduction of IgA is thought to play a role in the pathogenesis of primary IgA nephropathy. CD4+CD25+Fox3P regulatory T cells are instrumental in suppressing adaptative immune responses, including B cells production of immunoglobulins. We, the researchers at Centre Hospitalier Universitaire de Saine Etienne, will test the hypothesis that IgA production in patients with IgA nephropathy is dysregulated because of a quantitative and/or qualitative defect of CD4+CD25+FoxP3+ regulatory T cells.