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Clinical Trials

Patients play a central role in research. ‎They are key partners in advancing medical knowledge that improves the lives of those living with kidney disease.

Current Studies

You can contribute by participating in one of our current research studies.

ADVOCATE: ANCA Associated Vasculitis (AAV) standard therapy includes cyclophosphamide and glucocorticoids (such as Prednisone). Glucocorticoid is the main treatment for this condition; however it comes with significant side effects such as infection. These adverse events highlight the need for other newer medical therapies, as well as new ways to reduce or eliminate the need for chronic (more than a few months) high dose glucocorticoid use in the treatment of patients with AAV.  Based on previous encouraging results from other clinical trials, a new therapy called CCX168 (avacopan) has the potential to be used as a treatment for AAV with potential safety and tolerability advantages and has shown to be at least as good as the standard of care regimen that includes high doses of glucocorticoid treatment, such as prednisone.  For more information, click here or email

C3G: A Randomized, Double-Blind, Placebo-Controlled, Phase 2 Study to Evaluate the Safety and Efficacy of Avacopan (CCX168) in Patients with C3 Glomerulopathy 

In C3 glomerulopathy, the complement system, which is part of the immune system, is not regulated appropriately. This leads to over-activation of the system, resulting in deposition of complement products in the filtration units of the kidney. Currently, there is no approved drug treatment for patients with C3 glomerulopathy. Immunosuppressive drugs such as cyclophosphamide, mycophenolate mofetil, and glucocorticoids, as well as biologics such as rituximab have been used with limited success.

One way to treat C3 glomerulopathy may be to regulate the action of a specific protein that is part of the complement system called C5a on its receptor C5aR. Avacopan is a drug that selectively targets this C5aR and blocks the activity of C5a. 

For more information, click here or email

DIAMOND Study: A study to assess the Renoprotective Effects of SGLT2 Inhibitor Dapagliflozin in Non-Diabetic Patients with Proteinuria: a Randomized Double Blind 6-Weeks Cross-Over Trial 

Although currently, patients with chronic kidney disease and high protein in their urine are receiving the best possible medication for their disease, many patients with non-diabetic kidney disease continue to lose kidney function due to high levels of protein loss in the urine.  Urine protein is an important marker of kidney injury and it is believed that lowering levels of urine protein may be related to protection of kidney function over time.  For this reason, better treatment strategies are required to decrease the protein loss and by doing so, slow kidney function loss. 

The main purpose of this study is to determine if dapagliflozin has potentially beneficial effects on lowering the level of urine protein in patients with non-diabetic kidney disease (membranous nephropathy, IgA nephropathy, focal sclerosis).

For more information, click here or email

EMPA-KIDNEY Study: A multicentre international randomized parallel group double-blind placebo-controlled clinical trial of EMPAgliflozin once daily to assess cardio-renal outcomes in patients with chronic KIDNEY disease 

Chronic Kidney Disease (CKD) is caused by many different things, including increasing age. Diabetes, high blood pressure, inflammation in the kidney and inherited diseases are the most common causes in Canada. It is known that people with CKD are both at risk of their kidney problem worsening and developing heart problems.

The purpose of this study is to find out if taking a single pill of empagliflozin every day prevents worsening of kidney disease or deaths from heart disease in people who have kidney disease. Empagliflozin has been shown to have beneficial effects on both the heart and kidney in diabetics. 

For more information, click here or email

The SPOR Canadian GN Registry (CGNR) and Translational Research Initiative  
GN is a group of rare diseases (<5 per 250,000 population), yet is a leading cause of kidney failure and accounts annually for close to 20 % of new cases of end stage kidney disease (ESKD) in Canada. Prevention of progression to kidney failure is possible, however there are several barriers and gaps in knowledge that challenge the ability to provide patients with individualized effective therapy. 

We are collaborating with other centers across Canada to address these challenges.  We will create a registry by enrolling a large group of patients across the country with these types of glomerulonephritis: MCD (minimal change disease), FSGS (Focal and segmental glomerulosclerosis), MN (Membranous nephropathy), Mesangioproliferative Glomerulonephritis (MPGN) or IgAN (Immunoglobulin A nephropathy).  Participation would involve a hospital visit twice a year over a 2 year period to collect medical information, demographics (such as age and gender), as well as blood and urine samples.  Having this source of data will be an invaluable resource for national collaborative translational research in this rare disease. 

For more information, click here or email

Testing: IgA nephropathy is one of most common reasons for kidney failure, especially in younger adults. Decreased kidney function, high blood pressure and the presence of protein in the urine (proteinuria) are the strongest risk factors for kidney failure. Current therapies include blood pressure control for patients with proteinuria and/or hypertension, but a substantial risk of kidney failure remains even when these therapies are given. This study will evaluate the long-term effectiveness and safety of oral methylprednisolone compared to matching placebo, in preventing kidney events in patients with IgA nephropathy and features suggesting a high risk of progression. For more information, click here or email

For more information regarding different types of clinical studies, reasons to participate and what to expect, please visit the PHSA website.  

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