Clinical Trials

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7 studies in Division of Nephrology and Hypertension in Rochester, MN.

  1. A Phase 2 Open-label Multi-centre Study to Evaluate the Efficacy and Safety of Oxabact® to Reduce Plasma Oxalate in Subjects With Primary Hyperoxaluria Who Are on Dialysis
    Rochester, Minn. View Summary

    A Phase 2 Open-label Multi-centre Study to Evaluate the Efficacy and Safety of Oxabact® to Reduce Plasma Oxalate in Subjects With Primary Hyperoxaluria Who Are on Dialysis

    Location:

    Rochester, Minn.

    Trial status:

    Open for Enrollment

    Why is this study being done?

    The purpose of this study is to determine if Oxalobacter formigenes is effective at lowering plasma oxalate levels in patients with primary hyperoxaluria who are on dialysis.

    NCT ID:

    NCT02000219

    IRB Number:

    13-009042

    Who can I contact for additional information about this study?

    Rochester: Tamara Evans 507-284-1004
                        


  2. EARLY DETECTION OF BROKEN HEARTS IN CANCER PATIENTS: BEVACIZUMAB, SUNITINIB AND HEART FAILURE
    Rochester, Minn. View Summary

    EARLY DETECTION OF BROKEN HEARTS IN CANCER PATIENTS: BEVACIZUMAB, SUNITINIB AND HEART FAILURE

    Location:

    Rochester, Minn.

    Trial status:

    Open for Enrollment

    Why is this study being done?

    A total of 100 individuals (50 receiving BVZ and 50 receiving Sunitinib) will be prospectively enrolled . (80 at Mayo Clinic [40 receiving BVZ and 40 receiving Sunitinib] and 20 at St. Boniface General Hospital (SBGH)). Patients receiving either BVZ 5mg/kg iv every 2-3 weeks for colorectal cancer or Sunitinib 50 mg po daily for advanced Metastatic renal cell carcinoma will be screened for potential eligibility in the study. For metastatic renal cancer treatments, Sunitinib doses are (oral) 50 mg once a day for 4 weeks followed by a two week off period. The six week cycle is then repeated. In case of toxicities observed with the dose, a 25% reduction in the daily dose during the "on" period is performed (37.5 mg). Patients will be studied at 7 time points: i) Baseline; ii) Day 1; iii) Day 5; iv) 4-6 weeks ; v) 3 months; vi) 6 months after the initiation of both drugs (BVZ and Sunitinib) ; and vii) 12 months after the initiation of BVZ drug only (Figure 1). Three visits (baseline, 4-6 weeks , and 3 months) are considered part of standard clinical care, and four visits are for research. At each visit, in addition to standard of care provided by the Oncologist, blood will be drawn to measure high sensitivity troponin-T (hsTnT) and Natriuretic-proBNP. The patients will also undergo a TTE with tissue velocity imaging (TVI), strain and left ventricular opacification (LVO) and myocardial perfusion at each time point. EndoPAT test will also be performed at baseline, and 3 months. The baseline, 4-6 weeks, and 3 month visits will be part of your standard clinical care and followup.

    NCT ID:

    NCT02086695

    IRB Number:

    12-005362

    Who can I contact for additional information about this study?

    Rochester: Sharon L Mulvagh, M.D. 507-284-9601
                        


  3. Biobank Protocol, Rare Diseases Clinical Research Network
    Rochester, Minn. View Summary

    Biobank Protocol, Rare Diseases Clinical Research Network

    Location:

    Rochester, Minn.

    Trial status:

    Open for Enrollment

    Why is this study being done?

    Biologic samples will be stored in the biobank from well characterized patients with primary hyperoxaluria, cystinuria, APRT deficiency, and Dent disease, and from their family members, for use in future research. This will help to advance our understanding of disease expression and the factors associated with kidney injury in these four diseases with the overall goal of developing new treatments to preserve kidney function and reduce nephrocalcinosis and stone formation.

    NCT ID:

    NCT02026388

    IRB Number:

    11-005413

    Who can I contact for additional information about this study?

    Rochester: Alicia M Meek 507-255-4347
                        Barbara M Seide 507-255-0387


  4. An Open, Non-interventional, Retrospective, Comparative, Multicenter Follow-up Study in Patients Included in the Previously Completed Clinical Study pc b305/04, to Assess a Longer-term Recurrence Rates in Patients After Hexvix® (Cysview®)Fluorescence Cystoscopy/Turb or White Light Cystoscopy/TURB
    Rochester, Minn. View Summary

    An Open, Non-interventional, Retrospective, Comparative, Multicenter Follow-up Study in Patients Included in the Previously Completed Clinical Study pc b305/04, to Assess a Longer-term Recurrence Rates in Patients After Hexvix® (Cysview®)Fluorescence Cystoscopy/Turb or White Light Cystoscopy/TURB

    Location:

    Rochester, Minn.

    Trial status:

    Open for Enrollment

    Why is this study being done?

    A previously completed pivotal clinical study PC B305/04 demonstrated reduced recurrence rates for patients with papillary bladder cancer who underwent Hexvix (Cysview) and white light cystoscopy and transurethral resection (TURB) of the bladder compared to patients who underwent white light cystoscopy and TURB alone. The present study is intended to investigate whether the improved initial detection and resection of bladder cancer lesions in patients with non-muscle invasive bladder cancer with Hexvix (Cysview) fluorescence cystoscopy/TURB will also lead to a longer-term reduction in recurrences compared to standard white light cystoscopy/TURB.

    NCT ID:

    NCT01166230

    Who can I contact for additional information about this study?

  5. MSC for Occlusive Disease of the Kidney
    Rochester, Minn. View Summary

    MSC for Occlusive Disease of the Kidney

    Location:

    Rochester, Minn.

    Trial status:

    Open for Enrollment

    Why is this study being done?

    To determine the safety and toxicity of intra-arterial infused autologous adipose derived mesenchymal stromal (stem) cells in patients with vascular occlusive disease of the kidney.

    NCT ID:

    NCT01840540

    IRB Number:

    12-009298

    Who can I contact for additional information about this study?

    Rochester: Beverly K Tietje, Associate 507-255-0401
                                             
             
             
           
  6. BIIB023 for Subjects with Lupus Nephritis
    Rochester, Minn. View Summary

    BIIB023 for Subjects with Lupus Nephritis

    Location:

    Rochester, Minn.

    Trial status:

    Open for Enrollment

    Why is this study being done?

    Survival of patients with systemic lupus erythematosus (SLE) has improved greatly in the last decade, but lupus nephritis remains an important cause of morbidity and mortality in these patients. Recent studies have shown that we current therapies up to 50% of the patients with lupus nephritis fail to reach primary renal remission outcomes.  Thus, there is a need for more effective therapies in patients with lupus nephritis.

    The primary objective of the study is to assess the efficacy of BIIB023, an inhibitor of TWEAK (TNF-related weak inducer of apoptosis), as an add-on treatment to standard therapy compared with placebo in combination with standard therapy in the treatment of subjects with active, biopsy-proven lupus nephritis.

    There is substantial therapeutic rationale for inhibiting TWEAK in lupus nephritis: blocking the binding of TWEAK to Fn14 (fibroblast growth factor-inducible 14), BIIB023 attenuates TWEAK/Fn14 signaling and the downstream cellular responses of this signaling cascade; TWEAK induces the expression of proinflammatory mediators in both mesangial cells and podocytes, as well as in renal tubules, which may promote glomerulonephritis and tubulointerstitial inflammation. Since inflammation is considered to be a key mediator of tissue damage, TWEAK may promote tissue damage in lupus nephritis by promoting the recruitment of inflammatory infiltrates. TWEAK also acts in concert with other cytokines to promote renal tubular cell death. Thus, TWEAK may play an important pathogenic role in glomerulonephritis by promoting a local inflammatory environment and inducing tissue damage leading to progression to both glomerulosclerosis and tubulointerstitial fibrosis.

    Elevated levels of urinary TWEAK are observed in subjects with active lupus nephritis. Analyses of urinary TWEAK demonstrated that urinary TWEAK levels in biopsy-proven lupus nephritis patients are significantly higher than those found in SLE non-lupus nephritis patients and healthy controls. A significant association was found between urinary TWEAK levels and lupus nephritis disease activity as measured by the renal Systemic Lupus Erythematosus Disease Activity Index. Urinary TWEAK levels are also higher in patients undergoing a renal flare as compared with those with stable chronic renal disease and in patients undergoing renal as opposed to non-renal flare.

    Because TWEAK may promote multiple pathogenic activities locally in the kidney, it represents a promising target for therapeutic intervention. Inhibition of the TWEAK/Fn14 pathway with anti-TWEAK monoclonal antibodies has proven effective in multiple animal models of inflammatory diseases, suggesting that TWEAK blockade by BIIB023 may be clinically beneficial in lupus nephritis.

    The lack of a prominent impact on normal tissue homeostasis and adaptive immunity suggest that anti-TWEAK agents may have an attractive profile with respect to susceptibility to opportunistic infections and may therefore be combined with existing immunosuppressive therapies for LUPUS NEPHRITIS to achieve a novel more effective therapeutic approach without increased risk of infection.

    IRB Number:

    11-008028

    Who can I contact for additional information about this study?

    Fernando C. Fervenza, M.D., 507-266-7083, fervenza, fernando @mayo.edu
    Shirley Jennison, 507-255-0231, jennison.shirley@mayo.edu
  7. Nephrotic Syndrome Study Network Under the Rare Diseases Clinical Research Network
    Rochester, Minn. View Summary

    Nephrotic Syndrome Study Network Under the Rare Diseases Clinical Research Network

    Location:

    Rochester, Minn.

    Trial status:

    Open for Enrollment

    Why is this study being done?

    Idiopathic Nephrotic Syndrome (NS) is a rare disease syndrome responsible for approximately 12% of all causes of end-stage kidney disease (ESRD) and up to 20% of ESRD in children. Treatment strategies for Focal and Segmental Glomerulosclerosis (FSGS), Minimal Change Disease (MCD) and Membranous Nephropathy (MN), the major causes of NS, include high dose prolonged steroid therapy, cyclophosphamide, cyclosporine A, tacrolimus, mycophenolate mofetil and other immunosuppressive agents, which all carry significant side effects. Failure to obtain remission using the current treatment approaches frequently results in progression to ESRD with its associated costs, morbidities, and mortality. In the North American Pediatric Renal Trials and Collaborative Studies (NAPRTCS) registry, half of the pediatric patients with Steroid Resistant Nephrotic Syndrome required renal replacement therapy within two years of being enrolled in the disease registry. FSGS also has a high recurrence rate following kidney transplantation (30-40%) and is the most common recurrent disease leading to allograft loss. The prevailing classification of Nephrotic Syndrome categorizes patients into FSGS, MCD, and MN, if in the absence of other underlying causes, glomerular histology shows a specific histological pattern. This classification does not adequately predict the heterogeneous natural history of patients with FSGS, MCD, and MN. Major advances in understanding the pathogenesis of FSGS and MCD have come over the last ten years from the identification of several mutated genes responsible for causing Steroid Resistant Nephrotic Syndrome (SRNS) presenting with FSGS or MCD histopathology in humans and model organisms. These functionally distinct genetic disorders can present with indistinguishable FSGS lesions on histology confirming the presence of heterogeneous pathogenic mechanisms under the current histological diagnoses. The limited understanding of FSGS, MCD, and MN biology in humans has necessitated a descriptive classification system in which heterogeneous disorders are grouped together. This invariably consigns these heterogeneous patients to the same therapeutic approaches, which use blunt immunosuppressive drugs that lack a clear biological basis, are often not beneficial, and are complicated by significant toxicity. The foregoing shortcomings make a strong case that concerted and innovative investigational strategies combining basic science, translational, and clinical methods should be employed to study FSGS, MCD, and MN. It is for these reasons that the Nephrotic Syndrome Study Network is established to conduct clinical and translational research in patients with FSGS/MCD and MN.

    NCT ID:

    NCT01209000

    Who can I contact for additional information about this study?

    Rochester: Lori Riess 507-266-1047
                        Shirley Jennison 507-255-0231