Clinical Trials

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

  1. 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
                                             
             
             
           
  2. 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
  3. Correlation of Disease Expression With Specific Genetic Mutations in Primary Hyperoxaluria
    Rochester, Minn. View Summary

    Correlation of Disease Expression With Specific Genetic Mutations in Primary Hyperoxaluria

    Location:

    Rochester, Minn.

    Trial status:

    Open for Enrollment

    Why is this study being done?

    During your study visit, we will draw one tube, about two teaspoonfuls (1 to 1 ½ teaspoons for children), of blood from your arm to obtain white blood cells. These white blood cells will be used as a source of DNA for genetic testing. We will use the isolated DNA to try to identify the gene that is defective in Primary Hyperoxaluria by comparing it with the structure of genes in normal individuals, patients with Primary Hyperoxaluria, and family members of Primary Hyperoxaluria patients. In family members of primary hyperoxaluria patients, a 24 hour urine test may also be collected.

    NCT ID:

    NCT00589225

    IRB Number:

    434-03

    Who can I contact for additional information about this study?

    Rochester: Barbara Seide 507-255-0387
                        


  4. A Prospective Study of Airless Tubing in an Inpatient Acute Hemodialysis Unit in Hospitalized Patients in a Large Medical Center
    Rochester, Minn. View Summary

    A Prospective Study of Airless Tubing in an Inpatient Acute Hemodialysis Unit in Hospitalized Patients in a Large Medical Center

    Location:

    Rochester, Minn.

    Trial status:

    Open for Enrollment

    Why is this study being done?

    The introduction of unfractionated heparin (UFH), which prevents clotting of the extracorporeal circuit, was one of the key advances that led to the rapid development and expansion of hemodialysis use, and remains the mainstay in hemodialysis practice today. However, anticoagulation during hemodialysis of the patient at high risk for bleeding remains a frequently encountered problem in the nephrology practice. The need for anticoagulation to prevent clotting of the extracorporeal blood circuit and the need to prevent anticoagulation related bleeding complications in the patient has led to the development of numerous strategies; the safest from a bleeding standpoint being anticoagulant-free hemodialysis. Streamline® bloodlines (Medisystems® Corporation, Lawrence, MA) are designed to eliminate blood-air contact. A pressure pod measures arterial and venous pressures without any blood-air contact. The venous chamber is run without an air gap. It is also designed so that blood flows in a circular vortex manner. This airless system is thought to provide several benefits: improved dialysis efficiency and blood flow rates, reduced heparin use and clotting rates. The goal of this study is to prospectively examine the Streamline® airless tubing system in an inpatient setting and its association with clotting rates, and dialysis efficiency.

    NCT ID:

    NCT02086682

    IRB Number:

    13-003161

    Who can I contact for additional information about this study?

  5. A Multicenter, Randomized, Prospective, Open-Label Trial of Rituximab in the Treatment of Progressive IgA Nephropathy
    Rochester, Minn. View Summary

    A Multicenter, Randomized, Prospective, Open-Label Trial of Rituximab in the Treatment of Progressive IgA Nephropathy

    Location:

    Rochester, Minn.

    Trial status:

    Open for Enrollment

    Why is this study being done?

    Hypothesis: In patients with progressive IgA nephropathy an intravenous infusion of 1000 mg of rituximab on Day 1 and Day 15 and Days 168 and 182 is superior to conventional therapy in reducing 24 hour proteinuria, and slowing progression of chronic kidney disease. . 2.0 OBJECTIVES 2.1 Primary Efficacy Endpoints: Percentage of patients in each group achieving complete or partial response as defined below: Complete Response: At 12 months 1. < 300 mg proteinuria/24 hours Pediatric Criteria: First morning void urine protein: creatinine ratio <0.3 2. No greater than a 10% reduction in baseline estimated GFR as determined by MDRD (4 point) formula Partial Response: At 12 months 1) > 50% reduction in 24 hour proteinuria 2) No greater than a 25% reduction in baseline estimated GFR as determined by MDRD formula No Response: At 12 months 1. A 50% reduction, unchanged or increasing proteinuria over baseline levels will be considered no response 2. A greater than a 30% reduction in baseline estimated GFR as determined by MDRD formula 2.2 Primary Safety Endpoints: - Incidence of Infusion Related Reactions: Defined as the development of hypotension, generalized pruritus, chills/rigors, angioedema and/or bronchospasm. - Pulmonary Complications: Defined as a hypoxia, pulmonary infiltrates and/or acute respiratory failure - Incidence of Major Infections: Defined as the development of pneumonia, complicated UTI/Pyelonephritis, Sepsis, and Meningitis. - Development of Progressive Multifocal Leukoencephalopathy (PML) 2.3 Secondary Exploratory Efficacy Endpoints: A) For patients in Groups 1 & 2 consenting to a repeat kidney biopsy at 12 months, a secondary endpoint will include the percentage of patients in experiencing a 25% increase in cortical fibrosis. The response rate will be semi-quantified by the change in cortical fibrosis as measured by changes in Sirius Red staining of interstitial collagen. A patient will be considered a complete or partial response or no response according to the following criteria: Complete: Less than 10% rise in cortical fibrosis as measured by Sirius Red staining and digital image analysis Partial: Rising cortical fibrosis > 10% but less than 25% No Response: Greater than 25% rise in cortical fibrosis over baseline levels-(if patient consents to repeat kidney biopsy)

    NCT ID:

    NCT00498368

    IRB Number:

    07-001944

    Who can I contact for additional information about this study?

    Rochester: Fernando C. Fervenza, M.D., Ph.D. 507-266-7961
                        Shirley A Jennison 507-255-0231


  6. 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


  7. Screening for Dent Disease Mutations in Patients With Proteinuria
    Rochester, Minn. View Summary

    Screening for Dent Disease Mutations in Patients With Proteinuria

    Location:

    Rochester, Minn.

    Trial status:

    Open for Enrollment

    Why is this study being done?

    During this study visit, the investigator will draw one tube, about two teaspoonfuls (1 to 1 ½ teaspoons for children), of blood from your arm to obtain white blood cells. These white blood cells will be used as a source of DNA for genetic testing. We will use the isolated DNA to try to identify the gene that is defective in Dent Disease by comparing it with the structure of genes in normal individuals, patients with Dent Disease, and family members for Dent Disease.

    NCT ID:

    NCT01783795

    IRB Number:

    10-006442

    Who can I contact for additional information about this study?

    Rochester: Barbara M Seide 507-255-0387
                        Mayo Clinic Hyperoxaluria Center 800-270-4637


  8. Role Of Phosphorus And FGF 23 In Patients With Dent Disease
    Rochester, Minn. View Summary

    Role Of Phosphorus And FGF 23 In Patients With Dent Disease

    Location:

    Rochester, Minn.

    Trial status:

    Open for Enrollment

    Why is this study being done?

    Patients with Dent disease have suppressed levels of FGF 23 which contributes to hypercalciuria, kidney stones, nephrocalcinosis and renal failure. Supplementation with phosphorus may reduce hypercalciuria.

    NCT ID:

    NCT02016235

    IRB Number:

    13-004774

    Who can I contact for additional information about this study?

    Rochester: Barbara Siede 800-270-4637
                        Alicia M Meek 800-270-4637


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