Active clinical trials for "Nephritis"

The aim of this study was to evaluate whether C4d is a better biomarker and examine whether C4d plasma levels correlate with treatment response and C4d kidney deposition in systemic lupus erythematosus (SLE) with lupus nephritis (LN).

This study investigate mycophenic acid (MPA) pharmacokinetics and pharmacogenomics and their impact on the clinical outcomes in lupus nephritis (LN) patients. Lupus nephritis patients (both active or inactive) will be recruited. MPA levels will be checked at 1, 2, 4, 8, 10, 12 hrs after MMF administration by an enzymatic assay upon recruitment, then at 6-months' intervals and also when clinically significant events occurred. The MPA levels will be correlated with clinical parameters and outcomes. Pharmacogenomics studies will also be carried out and correlated with MPA exposure and clinical outcomes.

Cyclophosphamide is widely used in the treatment of cancer and autoimmune diseases such as lupus nephritis. However, there is considerable variability in the response to cyclophosphamide treatment. Cyclophosphamide is a pro-drug that requires initial activation by CYP liver enzymes. Recent clinical studies have indicated a possible role of one CYP enzyme, CYP2C19 in this activation step. This enzyme has a genetic polymorphism (variants which lack functional activity) and people who have inherited these variants are poor metabolisers of certain drugs. The aim of this study is to determine whether response to therapy in a New Zealand population of lupus nephritis patients is determined by cyclophosphamide bioactivation (the metabolic phenotype) and CYP genotype. Currently there is no way of predicting a patient's response to cyclophosphamide. An understanding of the factors which contribute to the therapeutic failure in lupus nephritis is particularly important due to the high morbidity and mortality associated with this disease. There are other treatment options for lupus nephritis patients who fail to respond to cyclophosphamide. If successful, this study may help identify patients who are unlikely to respond to cyclophosphamide and thus should not be unnecessarily be exposed to the drug and may justify the use of newer, more costly immunosuppressive drugs such as mycophenolate mofetil and rituximab.

Henoch-Schönlein (HS) purpura is a common cause of renal glomerular injury in children. This condition is responsible for 10-15% of glomerulonephritis in children. The outcome is generally favorable, but up to 5% of patients develop kidney failure. The outcome of patients with kidney biopsy is less favorable with 7-50% of them progressing to chronic renal failure. Prevalence of HS is difficult to determine from literature. Annual incidence is estimated at 6.1 / 100,000 children in the Netherlands and up to 20.4 / 100 000 children in the United Kingdom. The proportion of children with HS who develop renal disease is difficult to determine because the numbers reported in the literature are variable and depend greatly on the type of the reporting center, whether or not specialized in pediatric nephrology. Thus the proportion of renal disease varies from 20% to 100% of children with a HS. The treatment of HS nephropathy (HSN) usually depends on the severity of histological lesions but histological classification is discussed and there is currently no consensus. Randomized studies are scarce and often do not allow to draw clear conclusions. A meta-analysis suggested a positive effect of corticosteroids on renal prognosis of severe forms but in this study the definition of renal disease was very heterogeneous. The only classification of the HSN recognized is from the International Study Group of Kidney Disease in Childhood (ISKDC) which is the following: grade I: minimal glomerula abnormalities, grade II: pure proliferation, grade III: crescents/ segmental lesions <50%,grade IV: crescents/ segmental lesions 50 to 75%, grade V: crescents/ segmental lesions > 75%, grade VI: pseudomesangiocapillary. However, this classification is questioned because it ignores other significant histological lesions such as interstitial fibrosis, tubular lesions, glomerular and interstitial inflammation, the appearance of crescents (segmental or totally encompassing the glomerulus, fibrous or cellular), segmental sclerosis, fibrosis and arteriolar appearance in immunofluorescence. There is currently no consensus on the criteria indicating the initiation of corticosteroid therapy whether oral or intra venous bolus. Some patients with severe clinical and / or histological initial presentation can evolve to remission spontaneously while others who have more moderate initial symptoms will evolve later to kidney failure. The management is therefore heterogeneous. In France, some centers perform a kidney biopsy almost always before starting treatment (or in the days following the start of treatment), while in other centers's treatment decision is based on the biology resulting from the glomerular disease, kidney biopsy being performed possibly in a second time in case of failure of the initial treatment. Principal objective of the study: assessment of the interest for the long term outcome of performing early a kidney biopsy (before the establishment of treatment or within 15 days after the start of treatment) in children with HSN compare to kidney biopsy performed later (depending on the response to initial therapy) or not performed. Secondary objective: assessment of the impact of early kidney biopsy (before the establishment of treatment or within of 15 days after the start of treatment) on the initial treatment HSN : does it modify or not the treatment started right before it (decided on clinical and biological criteria).

The aim of the study to assess the multifocal ERG (mfERG) changes in SLE patients treated with chloroquine in renal patients with comparison to SLE patients without kidney affection.

To determine the mechanisms and significances of synergistic effects of mycophenolic acid and LPS on IL-1β secretion by mononuclear

All patients with SLE that will be admitted in internal medicine department from August 2019 to January 2021 are eligible to be targeted and included in the study. The diagnosis of SLE will be according to the 1997 American college of Romatology revised criteria (Hochberg 1997). SLE patients with lupus nephritis will take kidney biopsy for standard care of management according to American college of Romatology guidelines 2012. The study will include three groups as follow: 1 - SLE patients with lupus nephritis. 2- SLE patients without lupus nephritis 3-A group of age and sex matched healthy individuals. The first group will represent the study group while the second and third groups group will be taken as control group Exclusion criteria: patients with 1- Chronic renal failure 2- Diabetes mellitus (DM) 3-Obstructive nephropathy 4- Renal artery stenosis 5- Hypertension 6- Heart failure 7- Hepatic diseases. 8- Existing intra renal A-V fistula. 9-Renal vein thrombosis Aims of the Research : Assessment of the renal resistive index in patients with lupus nephritis (LN), in SLE patients without lupus nephritis and in the healthy controls. Comparing the renal resistive index values in SLE patients with lupus nephritis with the SLE patients without LN and healthy controls. Assessment of the correlation between renal resistive index (RRI) and histological findings in renal biopsy in patients with lupus nephritis. Assessment of the correlation between renal resistive index (RRI) and renal function parameters (BUN, S Cr and eGFR). Evaluation of the role of RRI as predictor of treatment outcomes in patients with lupus nephritis. The study will be enrolled in three steps: The first step:comparison of renal artery resistive index(RRI) values between study group and controls. The second step :correlation between RRI of the patients with lupus nephritis and histological findings in renal biopsy and/ or kidney function parameters (BUN ,SCr , eGFR). The third step:the patients with lupus nephritis will be followed up for six month receiving the usual treatment according to KDIGO guidelines 2012 to demonstrate the response to treatment in patient with pathological RRI compared to with normal RRI

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.

study epidemiology of lupus nephritis patients admitted to nephrology unit inward or in outpatient clinic in Assiut Nephrology Unit

B-cell activating factor (BAFF), also known as B lymphocyte stimulator (BLyS) serves as a vital survival and differentiation factor for normal B-cell development. There is an inverse relationship between BAFF circulating levels and the percentage and number of circulating B cells. BAFF levels have been associated with the clinical activity of SLE in humans. BAFF plays a pathogenic role in SLE in part through T cell-dependent B cell autoantibody production. BAFF, has a role in the maintenance of memory B cells and promotes plasma cell survival. Treatment strategies involving BAFF blockade haven been studied in patients with SLE inducing overall improvement in disease activity, mainly in musculoskeletal and mucocutaneous domains leading to the approval of Belimumab for the treatment of patients with systemic lupus erythematosus without severe renal or neurological involvement. Antibodies against CD20 molecule, anti-CD20 antibodies (Rituximab), cyclophosphamide (CYC), and mycophenolate (MMF) have all been used for the treatment of different manifestations of systemic lupus erythematosus and both moderate and severe activity. Baseline C4 level, early normalization of complement, and reduction in proteinuria have been shown to predict renal response to therapy with MMF or CYC in lupus nephritis. With Rituximab (RTX), B cell depletion has been associated with response to treatment and relapse prediction. The elevation of serum BAFF levels after B cell depletion with RTX in SLE are associated with anti-double-stranded DNA antibody levels and disease flare. The rise of BAFF is probably due to the decrease in its receptors leading to a release of BAFF and a delayed regulation of BAFF mRNA transcription, both of which could favor the re-emergence of autoreactive B cells. It has been suggested that the rise in BAFF levels after anti-CD20 therapy might be related to flares of the disease. Additionally, the combination of anti-CD20 with anti-BAFF or antibodies against CD4, anti-CD4 antibody greatly reduces the number of splenic plasma cells in mouse models and anti-CD20 plus anti-BAFF has been proven to have a lasting benefit both in lupus-prone mice and in mice with established disease. Currently, there is a lack of information regarding MMF or CYC and BAFF levels without the use of concomitant RTX (for CYC) and in monotherapy (for MMF). We consider that it is fundamental to know the behavior of BAFF in patients with SLE after treatment with MMF or CYC bearing in mind the proposal of multiple experts of the possible use of sequential therapy of BAFF inhibition after B-cell depletion. Knowledge of the behavior of BAFF will allow me to better understand its implications in SLE and its therapy. If our hypothesis is true maybe, we can postulate the use of sequence therapy with Belimumab after CYC o MF induction with the proposal to reduce the flares.