1115498 / A study to correlate the epidemiological and clinical features of Steroid Resistance Nephrotic Syndrome including FSGS (Focal Segmental GlomeruloSclerosis) in childhood, in the UK, with genotype and to develop biomarkers of disease activity post transplantation
An open-label extension and safety monitoring study of patients with moderately to severely active crohn’s disease previously enrolled in the etrolizumab phase III protocol ga29144 (Study due to close 31/12/2019)
1304763 / A study of Clinical and Genetic Risk Factors for Encapsulating Peritoneal Sclerosis
A study of Clinical and Genetic Risk Factors for Encapsulating Peritoneal Sclerosis (Study due to close 30/11/2018)
1502050 / Development of a Pan UK Vasculitis Cohort to Analyse Variations in Disease Susceptibility and Outcomes
Primary systemic vasculitidies (PSV), encompassing Anti-Neutrophil Cytoplasmic Antibody (ANCA) associated vasculitis and medium vessel vasculitis, are relatively uncommon diseases, but have a propensity for renal involvement and account for a significant number of patients with both acute and chronic kidney disease. The aetiology of PSV is unknown and current therapies are non-specific and associated with major side effects. Outcome data for such patients have comprised small cohort studies from single centres. Understanding the factors that influence disease outcome and the impact different therapies have outside of clinical trials can only be achieved using a larger number of patients, accrued from multiple different units.
We propose to establish the first pan-UK PSV dataset, which will collect regular returns regarding patient recruitment and outcome from all participating centres. This will facilitate investigation of disease associations, outcomes and demographic trends for the UK PSV population. We will test the hypothesis that disease incidence is increasing in Indo-Asians and why the outcome may be different among different ethnic groups, as well as investigating contemporary outcomes with modern immunosuppressive protocols. In addition, we will combine clinical phenotype with genetic studies. Specifically we will investigate genetic variation between ethnic groups by looking at variations in DNA sequences that can help to explain differences in disease susceptibility. These are investigated using many DNA specific markers, called single-nucleotide polymorphisms (SNPs) whose expression will be compared between patients from different ethnic groups.
Finally, we will be able to record the outcome of all patients treated with novel therapeutics, thus eliminating the significant reporting bias that exists. This will allow individual investigators to carry out particular projects mining the dataset. (Study due to close 31/12/2019)
1506108 / National Studies of Rare Kidney Diseases
National Studies of Rare Kidney Diseases (Study due to close 31/03/2019)
1610316 / A Phase 3b, Multi-center, Open-label Trial to Evaluate the Long Term Safety of a Titrated Immediate-release selective arginine vasopressin type 2 receptor antagonist (30 mg to 120 mg/day, Split dose) in Subjects with Autosomal Dominant Polycystic Kidney Disease (protocol 156-13-211)
A Phase 3b, Multi-center, Open-label Trial to Evaluate the Long Term Safety of a Titrated Immediate-release selective arginine vasopressin type 2 receptor antagonist (30 mg to 120 mg/day, Split dose) in Subjects with Autosomal Dominant Polycystic Kidney Disease (protocol 156-13-211) (Study due to close 31/12/2018)
1706439 / Microcirculatory function in peritoneal dialysis
For people with kidney failure the work of the kidneys is done by dialysis. Peritoneal dialysis is one form of dialysis that patients can do every day in their own home. A plastic tube placed surgically in the abdominal wall allows dialysis fluid to be drained into the abdominal cavity. Your body has toxins which are normally removed by the kidneys and also excess fluid it doesn’t need. In peritoneal dialysis these both pass through a natural membrane in the abdomen and go into the dialysis fluid. This is then drained out and discarded. The speed at which the toxins leak across into the dialysis fluid varies in different people. Contrary to expectations, however, the quicker the toxins move across the membrane (fast transporters), the faster the peritoneal dialysis process fails.
We will do the research at the universities of Exeter and Cardiff. We will get help from specialist kidney doctors, nurses, and of course, patients on peritoneal dialysis.
Some patients are ‘fast transporters’. They have more complications from peritoneal dialysis. The techniques we are testing will let us check if these people have problems with ‘leaky’ blood vessels in the rest of their body.
The aim of this study is to increase our knowledge of how peritoneal dialysis works and fails. When peritoneal dialysis stops working patients have to change to a different form of dialysis. This is called haemodialysis. They have to be connected to a machine at the hospital three times a week. This has a big effect on their lifestyle and independence.
We hope our work will eventually lead to treatments which will prolong the time patients can stay on peritoneal dialysis and maintain their quality of life and independence. (Study due to close 08/02/2019)
1706448 / aHUS
Phase 3, Randomized, Open-Label, Active-Controlled Study of ALXN1210 Versus Eculizumab in Complement Inhibitor Treatment-Naïve Adult and Adolescent Patients with Atypical Hemolytic Uremic Syndrome (aHUS) (Study due to close 13/02/2020)
1706453 / BISTRO
Background: Most patients who develop kidney failure choose unit-based haemodialysis treatment. Dialysis removes waste products and excess fluid from the blood when the kidneys stop working properly. Haemodialysis involves diverting blood to a machine to be cleaned.
One of the main functions of dialysis is to control the amount of fluid in the body. Too much fluid can lead to raised blood pressure that damages the heart and increases the risk of stroke, and may cause fluid to collect in the lungs leading to breathing difficulties. Too little fluid causes dehydration, cramps and low blood pressure and more rapid or complete loss of any remaining kidney function. Bioimpedance is a simple, bedside measurement giving information about body composition, specifically how much excess fluid is present. Clinicians can use this to guide how much fluid should be removed from the body with the normal clinical assessment of the amount of fluid in the body, but it is not known if this results in better decisions and outcomes for patients.
Research aims: To test whether taking regular measurements with a bioimpedance device, which gives information about body composition, improves outcomes for people who have newly started haemodialysis treatment for kidney failure. In particular, the study aims to see if this helps patients maintain their remaining kidney function, as this is associated with improved survival, fewer symptoms of kidney failure, fewer side effects of dialysis treatment and a better quality of life including confidence in managing their health, and cost benefit analysis.
Design and methods: People starting haemodialysis as an outpatient with some remaining kidney function will be invited to participate in a clinical trial that compares current best practice with the same but additionally guided by regular bioimpedance measurements. The study will randomise 516 patients from 30 dialysis units across the UK. (Study due to close 30/06/2018)
1710508 / ANCA
A Randomized, Double-Blind, Placebo-Controlled, Phase 3 Study to Evaluate the Safety and Efficacy of CCX168 (Avacopan) in Patients with Anti-Neutrophil Cytoplasmic Antibody (ANCA)-Associated Vasculitis Treated Concomitantly with Rituximab or Cyclophosphamide/Azathioprine (Study due to close 31/12/2018)
1710511 / PAVE trial
Paclitaxel assisted balloon Angioplasty of Venous stenosis in haEmodialysis access: The PAVE trial. A multicentre double-blind randomised controlled trial in haemodialysis patients with a stenosis in a native arteriovenous fistula. (Study due to close 30/09/2018)
1712549 / A 6-year, Multicentre, Non-interventional, Post-authorisation Safety Study for Patients Prescribed JINARC® for Autosomal Dominant Polycystic Kidney Disease
A 6-year, Multicentre, Non-interventional, Post-authorisation Safety Study for Patients Prescribed JINARC® for Autosomal Dominant Polycystic Kidney Disease (Study due to close 31/12/2019)
1802580 / Glycaemic Variability in Peritoneal Dialysis
For people with kidney failure the work of the kidneys is done by dialysis. Peritoneal dialysis is one form of dialysis that patients can do every day in their own home. A plastic tube placed surgically in the abdominal wall allows dialysis fluid to be drained into the abdominal cavity. Toxins that would normally be removed by the kidneys and excess fluid the body doesn’t need pass through a natural membrane in the abdomen into the dialysis fluid. The dialysis fluid is then drained out and discarded.
People on dialysis are at much higher risk of developing heart disease than the general population. One factor which may contribute to this is the large amount of sugar that is used in the peritoneal dialysis fluid. The sugar is required in the dialysis fluid to stimulate the movement of toxins out of the body. But some of the sugar in the fluid passes from the abdomen into the body. We know that uncontrolled sugar levels in the blood can lead to diabetes, heart attacks and strokes.
We will be asking patients who don’t have diabetes to wear a small glucose sensor on their arm for 72 hours. Half of these patients will be on peritoneal dialysis and the other half will be patients with declining kidney function who are not yet on dialysis This will allow us to measure what effect the process of peritoneal dialysis has on blood sugar levels.
We hope that a greater understanding of this process will help us to develop treatments which may be able to protect against some of these damaging effects. And ultimately improve patients’ quality of life. (Study due to close 31/08/2018)
1803564 / The SIMPLIFIED Registry Trial
Vitamin D deficiency is common in kidney failure, and is a strong predictor of death from cardiovascular disease, infections and cancer. Dialysis patients typically receive pre-activated vitamin D, since it used to be thought that only the kidneys activate vitamin D. However, this increases blood calcium concentrations and may paradoxically make vitamin D deficiency worse. International treatment guidelines now recommend that kidney patients receive inactive vitamin D (known as cholecalciferol), since we now know that every organ activates vitamin D as required, even in kidney failure. However, this approach has not yet been tested in a trial. We will test whether supplementation with cholecalciferol increases survival in UK dialysis patients.
We will randomly assign adult UK dialysis patients to cholecalciferol or standard care.
We will determine the number of deaths over time in the two groups, to establish whether cholecalciferol improves survival. Whether patients are alive or dead at the end of the study will be determined from the national deaths register. We will also measure any differences in survival free from cardiovascular events, infections and cancers, the three leading causes of death in those on dialysis. We will use questionnaires to compare the quality of life of those in the two groups.
Currently only 68% of patients survive 3 years or more on dialysis. Assuming that this will be the case in the control group, we would need to witness 2200 deaths during the study to determine with a sufficient degree of certainty whether cholecalciferol improves survival. We estimate that this would require the inclusion of 4200 patients, followed for a total study duration of approximately 7 years. Put differently, this trial is designed to detect whether cholecalciferol has a clinically relevant effect by saving 4 or more lives for every 100 patients treated. (Study due to close 31/03/2020)
1804578 / Natural History Study of C3 Glomerulopathy
C3 glomerulopathy (C3G) describes a rare renal disease characterised by the presence of C3 in the filtering units (glomeruli) in the kidney. C3 accumulation in the kidney results from over-activation of part of the immune system known as the complement alternative pathway. C3 accumulation results in inflammation in the glomeruli (glomerulonephritis) and this inflammation results in permanent damage in 30-50% of patients within 10 years of diagnosis, with these patients requiring dialysis or a transplant.
Currently there is no available cure for C3G and there is no approved treatment to prevent disease progression. Patients have a variable course of disease which is difficult to predict and treat. There is a need to understand better the clinical course of C3G, that is its natural history. Natural history refers to the clinical course of the condition in the setting of current standard of care. This includes supportive therapy (blood pressure control, anti-proteinuria agents) and in some individuals, immunosuppression.
The aim of this study is to determine the pathological spectrum of C3G, using clinical features available at diagnosis, including renal biopsy results, which will enable us to meaningfully stratify patients with C3G into different prognostic groups and/or treatment groups. We aim to determine precise histological and clinical indicators and biomarkers of disease that my likely predict therapeutic response. This is extremely important to patients with C3G. In order to achieve this we aim to collect a large group of patients from different centres around the world.
We use the term C3 glomerulopathy to encompass all related complement-derived pathological sub-types: C3 glomerulonephritis, dense deposit disease, idiopathic membranoproliferative glomerulonephritis, atypical post-infectious glomerulonephritis, unspecified C3 glomerulopathy (Study due to close 31/12/2019)