View clinical trials related to Nephritis.
Filter by:This is a multi-center study to evaluate the safety, tolerability, PK, PD, and clinical activity of itolizumab (EQ001) in subjects with Systemic Lupus Erythematosus with or without Active Proliferative Lupus Nephritis
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 : 1. Assessment of the renal resistive index in patients with lupus nephritis (LN), in SLE patients without lupus nephritis and in the healthy controls. 2. Comparing the renal resistive index values in SLE patients with lupus nephritis with the SLE patients without LN and healthy controls. 3. Assessment of the correlation between renal resistive index (RRI) and histological findings in renal biopsy in patients with lupus nephritis. 4. Assessment of the correlation between renal resistive index (RRI) and renal function parameters (BUN, S Cr and eGFR). 5. 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
The purpose of this study is to evaluate the safety and effectiveness of BMS-986165 compared with placebo with regard to measures of kidney function in participants with lupus nephritis (LN).
Glomerulonephritis (GN) generates an enormous individual and social economic burden. However, the therapeutic options are largely based on clinical and pathological parameters and the individual response to therapy or prognosis is uncertain. Recently, along with advances in molecular analysis and computational bioinformatics, genomic data from human renal biopsies could provide a strong foundation for the future of precision medicine in nephrology. In response to a request for applications by the Ministry of Health and Welfare of Korea for the creation of Clinical Research Registry, multi-center N network has been established for prospective cohort with kidney biopsy samples (KORNERSTONE). Through this Network the investigators hope to understand the fundamental biology of glomerulonephritis and aim to bank long-term observational data and corresponding biological data including genomic data from kidney tissues, and kidney pathologic data which is digitalized This database is archived to a web-based platform to access easily and further enrich for researchers.
Lupus is an autoimmune disease affecting mainly young women (9/1). Lupus nephritis (LN) occurs in 30% of the cases of lupus and is associated with end stage renal disease (ESRD) in 17 to 25% of cases after 10 years. Overall, nearly 7% of lupus patients will develop ESRD due to LN. Historically, 5-year survival after LN was lower than 20%. Nowadays, 45% of patients suffer from multiple relapses that are associated with an intermediate risk of ESRD. When ESRD occurs, lupus activity decreases progressively to reach a stable extinct state. At this stage it is possible to stop all medications to control lupus, without any flare of lupus activity. Lupus extinction following ESRD corresponds to a state of complete remission. Obtaining such a result before ESRD would avoid damages to several organs and side effects of immunosuppressive therapy. Understanding the mechanisms responsible for lupus extinction following ESRD is an innovative approach to decipher lupus pathophysiology. The objective of the study is to identify the mechanisms responsible for lupus extinction and to propose new therapeutic options based on these new mechanisms. Mechanisms responsible for lupus extinction are unknown. Lupus extinction depends on the duration of ESRD. Accumulation of several toxins that kidneys would normally eliminate in the urine is a hallmark of ESRD. Such toxins are called "uremic toxins" since they accumulate during "uremia" (ESRD). They affect biological systems such as fertility and immunity that are both closely related to lupus pathophysiology. The investigators hypothesize that studying LN extinction after ESRD will provide novel therapeutic targets to extinct lupus before ESRD. To this end, they will investigate several non-exclusive hypotheses based on previous findings of our consortium, or issued from clinical observations: the sexual dysfunction hypothesis and the ESRD-associated immune cells dysfunction hypothesis. In parallel, they will conduct an open screening of new mechanisms underlying the lupus extinction through the characterization of the differential gene expression profile associated with lupus extinction in patients undergoing dialysis.
A randomized open-label study of fixed-dose versus concentration-controlled mycophenolate mofetil for treatment of active lupus nephritis.
This protocol seeks to assist biorepositories/biobanks in distributing their stored specimens and data to researchers that will actually utilize them to advance medicine and technology.
Glomerulonephritis is an important manifestation in about 1/2 of patients with Systemic Lupus Nephritis (SLE; lupus). Despite recent national guidelines recommending use of induction therapy with high-dose corticosteroids and immunosuppressive agents, followed by prolonged maintenance therapy, up to 1/3 of these patients continue to have active nephritis and ongoing protein in the urine (proteinuria). It has long been recognized that both the level and chronicity of proteinuria in patients with lupus nephritis are associated with disease severity and with long-term prognosis, including the possibility of progression to complete kidney failure, which may occur in about 1/4 of patients. Pentoxifylline (PTX) is an oral medication introduced 45 years ago for treatment of vascular insufficiency. It has also recently been found to reduce proteinuria in patients with diabetic nephropathy. The mechanism of this unexpected and intriguing finding is not certain, but may in part involve inhibiting the production of TNF-alpha, an inflammatory cytokine known to be present in urine and kidneys of patients with lupus nephritis. Our hypothesis is that this inexpensive, generic drug, PTX, can significantly reduce proteinuria in patients with lupus nephritis. To test this hypothesis, we plan to initiate a 6-month, double-blind, placebo-controlled randomized clinical trial of PTX or placebo in 40 patients with active lupus nephritis. This trial will include 6-8 patients from each of 5 different academic medical centers that specialize in the treatment of lupus nephritis. Our primary objective of this trial will be to measure urine protein each month to determine the extent to which PTX is able to reduce urine protein, and how rapidly this occurs. Concurrently, we will carefully follow these patients each month to determine whether PTX administration is also associated with stabilization of renal function, or with improvement in other manifestations of lupus, such as clinical disease activity or abnormal laboratory findings. A major secondary objective will be to explore the possible mechanism(s) whereby PTX reduces proteinuria. For this purpose, we will use the monthly urine specimens to measure TNF-alpha, and levels of several other proteins (IL-1, IL-6, IL-2, MCP-1, TGF-beta, PDGF, and IFN-alpha) that have been shown to contribute to inflammation and scarring in lupus nephritis. Comparison of levels of these inflammatory proteins with level of protein in the urine should help us to determine whether one or more of these proteins is a contributor to the severity or persistence of lupus nephritis. This information may also allow us to learn whether repeated measurements of these proteins can serve as biomarkers to assist in the ongoing management of patients with lupus nephritis. Finally, we hope to eventually measure levels of these inflammatory proteins in blood samples from the patients, to determine if PTX treatment can suppress (or enhance) such levels, and whether these changes are associated with reduced lupus disease activity, or improvement in other manifestations of lupus. Ultimately, it is our hope that the data from this clinical trial using a generic repurposed drug will permit us to conclusively confirm that PTX can significantly reduce proteinuria in patients with lupus nephritis, which would be of great benefit for the thousands of people who suffer with this most severe type of lupus.
Systemic lupus erythematosus (SLE) is a chronic autoimmune disease characterized by the production of multiple autoantibodies and accumulation of immune complexes resulting in systemic inflammatory response and tissue damage. Although the underlying mechanisms are complex, defects in dying cells elimination are likely to contribute to autoantigen overload and development of autoimmunity. Molecules important in damaged cell clearance, such as early complement components, may thus have a protective role. According to this hypothesis, deficiencies in C1q and MBL, the recognition proteins of the classical and lectin pathways of complement; are associated with increased susceptibility to SLE. In the proposed project, the investigators will investigate the involvement of another related recognition protein, ficolin-3, which activates the complement lectin pathway and recognizes necrotic cells. The investigators have shown in a recent study a significant association between the presence of anti-ficolin-3 antibodies and active nephritis in patients with SLE. However, the possible involvement of anti-ficolin-3 antibodies in the pathogenesis of SLE and particularly in lupus nephritis (LN) remains to be elucidated. This project plans to investigate the role of ficolin-3 and ficolin-3 autoantibodies in LN. The study associates two aspects, aiming at deciphering the role of anti-ficolin-3 antibodies in dying cells recognition and investigating the role of ficolin-3 in renal tissue damage. This pilot study will be performed for 14 patients with active LN on serum and renal biopsy, realized for routine patient care. The investigators will explore the effect of anti-ficolin-3 antibodies purified from the patient serum on ficolin-3-dependent necrotic cells recognition, in relation with possible altered clearance of dead cells, which is an important hypothesis of the pathogenesis of SLE. The investigators will also investigate ficolin-3 deposition in renal biopsy, which may contribute to the local formation of immune complexes, leading to complement activation and subsequent inflammation and tissue injury.
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.