Active clinical trials for "Glomerulonephritis"

It has recently been described the presence of a urinary inflammatory signature in patients with cystinuria, the most common cause of renal lithiasis of genetical origin. These data are very innovative in this pathology but deserve further studies to establish the specificity of this inflammatory signature in patients with cystinuria compared to other nephropathies and other renal lithiasis diseases. Moreover, the effect of the usual treatment of cystinuria (namely urine alkalanization) on urinary inflammatory biomarkers deserves to be tested. The objectives of the present study are: i) To study the urinary inflammatory profile by mass spectrometry (a very efficient tool to detect and identify proteins) in patients with cystinuria and in patients with lithiasis of other origin and in patients with inflammatory renal disease ; ii) To study the potential effect of urine alkalinazation with potassium citrate (usual treatment according to European recommendations) on the inflammatory signature of patients with cystinuria. To this aim, urine of non treated cystinuric patients will be collected before treatement initiation and 3 months after the start of the alkalizing treatment.

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.

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.

OBJECTIVES: I. Determine whether allelic differences associated with the fourth component of complement, type-1 complement receptor expressed on erythrocytes, and Fc receptor FcgRIII contribute to the pathogenesis of IgA glomerulonephritis (IgA-N). II. Compare genetic anomalies of these key components in immune complex processing and clearance between juvenile vs adult onset IgA-N vs normal controls.

Urinary CD4+ and CD8+ T lymphocytes may predict renal flares in patients with inactive ANCA-associated vasculitis and thus serve as early non-invasive biomarkers. Urine samples of patients with inactive renal ANCA-vasculitis will be analysed by flow cytometry and compared to clinical outcome after 6 months.

Problems of compatibility between a mother and her child are frequent. The most well-known case can be illustrated by the fetomaternal blood group incompatibility (rhesus factor) which can induce severe anemia of the fetus. The investigators recently proved that incompatibility between mother and child can concern an organ leading to a tissular alloimmunization. For example, neonatal membranous glomerulonephritis (a kidney disease) can result from this mechanism. The purpose of this network is to detect and study neonatal diseases induced by tissular fetomaternal alloimmunization. The detection of these diseases will be performed by the mother's serum analysis.

The purpose of this ongoing study (Part II) is to estimate the incidence of acute rheumatic fever, rheumatic heart disease, acute post-streptococcal glomerulonephritis (kidney disease), and invasive group A streptococcal (GAS) disease (strep infection) in Fiji to help develop better treatments and vaccines. Group A streptococcal disease is caused by the bacterium group A streptococcus. It is commonly found in the nose and throat of normal healthy adults and children, and can cause illness. The bacterium is spread by close contact with patients or carriers, through things like coughing, sneezing, kissing, or sharing a drink and can cause a wide variety of illnesses. These illnesses may be a sore throat, skin sores, and less commonly acute rheumatic fever or kidney disease. Participants of all ages will be recruited through the Colonial War Memorial and Lautoka Hospital. A blood sample will be collected from each study participant. Subject participation should be less than one day.

The prevalence of kidney scarring after UTI is approximately 5-57%. UTIs are caused mainly by bacteria that cause local and systemic immunological reaction that are accompanied by cytokines. These cytokines are a main factor in the inflammatory process. They are produced by leukocytes, macrophages, fibroblasts, endothelial cells and epithelial cells in the kidney tissue. Interleukin 6 and 8 (IL-6 IL-8) were found in high levels in the urine of children and adults who suffer from UTIs. Other studies on animals have found a relationship between inflammatory reaction and scarring in the kidney. We hypothesize that we will find a similar relationship between the level of IL-6, IL-8 in the urine during acute pyelonephritis in children and the probability of kidney scarring.

CryoKid is a no-profit, multi-center, single-arm, open-label, pilot study. The study aims to evaluate the tolerability of MK-8742 (Elbasvir) / MK-5172 (Grazoprevir) administrated for 12 weeks without Ribavirin in patients with HCV chronic hepatitis (G1b and G4) and cryoglobulinemic nephropathy.

Glomerulonephritis (GN) is one of the most important causes of kidney failure in Canada. These comprise a group of "rare" diseases (<5 per 250,000 population), yet GN is a leading cause of kidney failure and accounts annually for close to 20% of incident cases of end stage kidney disease (ESKD) in Canada. Prevention of progression to kidney failure is possible, however several barriers and gaps in knowledge challenge our ability to provide patients with individualized effective therapy. These include a lack of sensitive non-invasive tools for monitoring disease activity, prognosis, and response to therapy. A gap in understanding of the core molecular processes underlying the development and progression of GN, and a lack of cohesive networks for evaluation of novel treatment approaches contribute to a lack of targeted and personalized therapies for GN. To address these challenges we will create a national, multi-dimensional platform for application of human-based molecular research and advanced therapeutics in GN.