Clinical Trials

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

  1. Phase I Study of Autologous Mesenchymal Stem Cells in the Treatment of Atherosclerotic Renal Artery Stenosis

    Rochester, Minn. View Summary

    Phase I Study of Autologous Mesenchymal Stem Cells in the Treatment of Atherosclerotic Renal Artery Stenosis

    Location:

    Rochester, Minn.

    Trial status:

    Open for Enrollment

    Why is this study being done?

    Individuals with unilateral arterial occlusive disease will be treated to injured kidney with autologous cells.

    NCT ID:

    NCT01840540

    IRB Number:

    12-009298

    Who can I contact for additional information about this study?

  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. Treatment for Patients With Bilateral, Multicentric, or Bilaterally-Predisposed Unilateral Wilms Tumor

    Rochester, Minn. View Summary

    Treatment for Patients With Bilateral, Multicentric, or Bilaterally-Predisposed Unilateral Wilms Tumor

    Location:

    Rochester, Minn.

    Trial status:

    Open for Enrollment

    Why is this study being done?

    OBJECTIVES: I. To improve 4-year event-free survival (EFS) to 73% for young patients with bilateral Wilms tumor (BWT). II. To prevent complete removal of at least one kidney in 50% of patients with BWT by using prenephrectomy 3-drug chemotherapy induction with vincristine (vincristine sulfate), dactinomycin, and doxorubicin (doxorubicin hydrochloride). III. To evaluate the efficacy of chemotherapy in preserving renal units in children with diffuse hyperplastic perilobar nephroblastomatosis (DHPLN) and preventing Wilms tumor development. IV. To facilitate partial nephrectomy in lieu of nephrectomy in 25% of children with unilateral tumors and aniridia, Beckwith-Wiedemann syndrome (BWS), hemihypertrophy or other overgrowth syndromes, by using prenephrectomy 2-drug chemotherapy induction with vincristine and dactinomycin. V. To have 75% of patients with BWT undergo definitive surgical treatment by 12 weeks after initiation of chemotherapy. OUTLINE: PREOPERATIVE CHEMOTHERAPY: Patients receive preoperative chemotherapy based on radiographic stage in most cases and if a biopsy was performed then based on histology. VAD REGIMEN (stage I-IV bilateral Wilms tumor [BWT] with biopsy revealing favorable histology or no preoperative biopsy; stage I-III BWT with focal anaplasia; stage I BWT with diffuse anaplasia; or high-risk, stage III-IV unilateral Wilms tumor [WT] with contralateral nephrogenic rest [NR] or predisposition syndrome): Patients receive vincristine sulfate IV on days 1, 8, 15, 22, 29, and 36 (weeks 1-6) and dactinomycin IV and doxorubicin hydrochloride IV over 15-120 minutes on days 1 and 22 (weeks 1 and 4). REVISED UH-1 REGIMEN (stage IV BWT with focal anaplasia; stage II-IV BWT with diffuse anaplasia; or stage I-IV malignant rhabdoid tumor of the kidney): Patients receive vincristine sulfate IV on days 1, 8, and 15 (weeks 1-3); doxorubicin hydrochloride IV over 15-120 minutes on day 1 (week 1); cyclophosphamide IV over 1 hour on day 1 and on days 22-25 (weeks 1 and 4); carboplatin IV over 1 hour on day 22 (week 4); and etoposide phosphate IV over 1 hour on days 22-25 (week 4). EE-4A REGIMEN (high-risk, stage I-II unilateral WT with contralateral NR or predisposition syndrome or diffuse hyperplastic perilobar NRs [DHPLNR]): Patients receive vincristine sulfate IV over 1 minute on days 1, 8, 15, 22, 29, and 36 (weeks 1-6) and dactinomycin IV over 1-5 minutes on days 1 and 22 (weeks 1 and 4). Patients are evaluated at week 6. If partial nephrectomy is feasible, patients proceed to definitive surgery and lymph node sampling followed by postoperative therapy. If partial nephrectomy is not feasible, patients receive additional chemotherapy (as above with the same or a different set of regimen) followed by definitive surgery at week 12 and postoperative therapy OR patients proceed to a different chemotherapy regimen. POSTOPERATIVE THERAPY: Patients receive postoperative therapy according to histology after preoperative chemotherapy and according to the highest assigned risk for either kidney. EE-4A regimen (BWT with complete resection of all gross tumors at diagnosis with stage I-II favorable histology; BWT with complete response [CR] by imaging after 6 weeks of preoperative chemotherapy; completely necrotic stage I-II BWT; intermediate-risk stage I BWT; unilateral WT stage I-II with CR by imaging after 6-12 weeks of preoperative chemotherapy; completely necrotic stage I-II unilateral WT; or intermediate-risk stage I-II unilateral WT): Patients receive vincristine sulfate IV over 1 minute on days 43, 50, 57, 64, 85, 106, and 127 (weeks 7-10, 13, 16, and 19) and dactinomycin IV over 1-5 minutes on days 43, 64, 85, 106, and 127 (weeks 7, 10, 13, 16, and 19). DD-4A REGIMEN (intermediate-risk, stage II BWT; stage I BWT with blastemal predominance; or stage I unilateral WT with blastemal predominance): Patients receive vincristine sulfate IV over 1 minute on days 1, 8, 15, 22, 29, and 36 (weeks 1-6); dactinomycin IV over 1-5 minutes on day 1 (week 1); and doxorubicin hydrochloride IV over 15-120 minutes on day 22 (week 4). Patients then receive vincristine sulfate IV over 1 minute on days 43, 50, 57, 64, 85, 106, 127, 148, and 169 (weeks 7-10, 13, 16, 19, 22, and 25); dactinomycin IV over 1-5 minutes on days 43, 85, 127, and 169 (weeks 7, 13, 19, and 25); and doxorubicin hydrochloride over 15-120 minutes on days 63, 106, and 148 (weeks 10, 16, and 22). Some patients may also undergo radiotherapy. DD-4A REGIMEN AND RADIOTHERAPY (BWT with complete resection of all gross tumors at diagnosis with stage III-IV favorable histology, completely necrotic stage III-IV BWT; intermediate-risk, stage III-IV BWT; stage I BWT with diffuse anaplasia; stage I-III BWT with focal anaplasia; stage I unilateral WT with diffuse anaplasia; stage I unilateral WT with focal anaplasia; or intermediate-risk, stage III-IV unilateral WT): Patients receive DD-4A regimen as above. Patients also undergo concurrent radiotherapy. REGIMEN I (stage II BWT with blastemal predominance or stage II unilateral WT with blastemal predominance): Patients receive vincristine sulfate IV over 1 minute on days 43, 50, 57, 71, 78, 85, 92, 127, and 169 (weeks 7-9, 11-14, 19, and 25); doxorubicin hydrochloride IV over 15-120 minutes on days 43, 85, 127, and 169 (weeks 7, 13, 19, and 25); cyclophosphamide IV over 15-30 minutes on days 43, 64, 85, 106, 127, 148, and 169 (weeks 7, 10, 13, 16, 19, 22, and 25); and etoposide phosphate IV over 1 hour on days 64, 106, and 148 (weeks 10, 16, and 22). REGIMEN I AND RADIOTHERAPY (stage III-IV BWT with blastemal predominance or stage III-IV unilateral WT with blastemal predominance): Patients receive regimen I as above. Patients also undergo concurrent radiotherapy. REVISED UH-1 REGIMEN AND RADIOTHERAPY (stage IV BWT with focal anaplasia; stage II-IV BWT with diffuse anaplasia; stage IV unilateral WT with focal anaplasia; stage II-IV unilateral WT with diffuse anaplasia; and stage I-IV malignant rhabdoid tumor of the kidney; or DHPLNR with anaplasia): Patients receive vincristine sulfate IV over 1 minute on days 64, 71, 78, 85, 92, 99, 148, 155, 162, 190, 197, and 204 (weeks 10-15, 22-24, and 28-30); doxorubicin hydrochloride IV over 15-120 minutes on days 64, 85, 148, and 190 (weeks 10, 13, 22, and 28); cyclophosphamide IV over 15-30 minutes on days 43-46, 64, 85, 106-109, 127-130, 148, 169-172, and 190 (weeks 7, 10, 13, 16, 19, 22, 25, and 28); carboplatin IV over 1 hour on days 43, 106, 127, and 169 (weeks 7, 16, 19, and 25); and etoposide phosphate IV over 1 hour on days 43-46, 106-109, 127-130, and 169-172 (weeks 7, 16, 19, and 25). Patients also undergo radiotherapy. VAD REGIMEN (DHPLNR with favorable histology WT with viable elements): Patients receive vincristine sulfate IV over 1 minute on days 43, 50, 57, 64, 71, and 78 (weeks 7-12) and dactinomycin IV over 1-5 minutes and doxorubicin hydrochloride IV over 15-120 minutes on days 43 and 64 (weeks 7 and 10). After completion of study treatment, patients are followed up periodically for 10 years.

    NCT ID:

    NCT00945009

    IRB Number:

    09-004942

    Who can I contact for additional information about this study?

    Rochester: Carola A. Arndt 507-538-7623
                        


  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


  8. Use of Tolvaptan to Reduce Urinary Supersaturation: a Pilot Proof of Principle Study

    Rochester, Minn. View Summary

    Use of Tolvaptan to Reduce Urinary Supersaturation: a Pilot Proof of Principle Study

    Location:

    Rochester, Minn.

    Trial status:

    Open for Enrollment

    Why is this study being done?

    In this study the investigators propose to use a daily dose of 45 mg (30 mg at 8 AM and 15 mg at 4 PM). This relatively small well-tolerated dose is likely to persistently increase urine volume and reduce urine supersaturation and to be well tolerated by patients with kidney stone disease and normal renal function (see below). The twice-daily (8 AM and 4 PM) regimen is designed to produce a maximal AVP inhibition on waking with a gradual fall-off of effect during the night. To this end, a higher dose is used in the morning, with a lower dose in the afternoon.

    NCT ID:

    NCT02096965

    IRB Number:

    11-001780

    Who can I contact for additional information about this study?

    Rochester: Ruth A. Kraft, Research Coordinator 507-266-8133
                        


  9. Clinical Trial to Slow the Progression of ADPKD

    Rochester, Minn. View Summary

    Clinical Trial to Slow the Progression of ADPKD

    Location:

    Rochester, Minn.

    Trial status:

    Open for Enrollment

    Why is this study being done?

    This study will determine whether certain blood pressure medications will slow cyst growth or keep kidneys functioning longer in patients with autosomal dominant polycystic kidney disease (ADPKD). The study will take place at several sites in the United States. The start date of the study has not yet been determined.

    NCT ID:

    NCT00067977

    Who can I contact for additional information about this study?

    Rochester: 507-284-0944
                        


  10. 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


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