xml: <clinical_study>
    <!-- This xml conforms to an XML Schema at:
      https://clinicaltrials.gov/ct2/html/images/info/public.xsd -->
    <required_header>
      <download_date>ClinicalTrials.gov processed this data on September 20, 2023</download_date>
      <link_text>Link to the current ClinicalTrials.gov record.</link_text>
      <url>https://clinicaltrials.gov/ct2/show/NCT05991245</url>
    </required_header>
    <id_info>
      <org_study_id>RNI/MATRIX</org_study_id>
      <secondary_id>F20221110095846</secondary_id>
      <secondary_id>2022-59</secondary_id>
      <nct_id>NCT05991245</nct_id>
    </id_info>
    <brief_title>French National Cohort MATRIX &quot;Renal and Systemic Thrombotic Microangiopathy&quot;</brief_title>
    <acronym>MATRIX</acronym>
    <official_title>French National Cohort MATRIX &quot;Renal and Systemic Thrombotic Microangiopathy&quot;</official_title>
    <sponsors>
      <lead_sponsor>
        <agency>University Hospital, Tours</agency>
        <agency_class>Other</agency_class>
      </lead_sponsor>
    </sponsors>
    <source>University Hospital, Tours</source>
    <oversight_info>
      <has_dmc>No</has_dmc>
      <is_fda_regulated_drug>No</is_fda_regulated_drug>
      <is_fda_regulated_device>No</is_fda_regulated_device>
    </oversight_info>
    <brief_summary>
      <textblock>
        Thrombotic microangiopathies (TMAs) are a diverse, rare but serious group of diseases.&#xD;
        Progress has been made regarding the epidemiology of TMA (Bayer CJASN 2019). It has been&#xD;
        shown that secondary TMAs account for 95% of cases, whereas primary TMAs (atypical hemolytic&#xD;
        syndromes (HUS) and thrombotic thrombocytopenic purpura (TTP)) account for only about 5%.&#xD;
  &#xD;
        However, in many cases, the pathophysiology, optimal management and prognosis of TMA remains&#xD;
        unclear and it has been shown that patients with TMA may have renal-limited TMA or renal and&#xD;
        hematological TMA (ie. With (mechanical anemia, thrombocytopenia, elevated LDH, decreased&#xD;
        haptoglobin, schistocytes). In most studies, kidney biopsies are not performed and the&#xD;
        diagnostic workup is uncomplete.&#xD;
  &#xD;
        As this is a rare disease, only a multicenter approach (&gt;20 centers) over a long period of&#xD;
        time (&gt;10 years), with adequate diagnostic workup including kidney biopsies can help us to&#xD;
        answer these questions (investigators in the present are usually members of the CNR-MAT (a&#xD;
        network of the TMA centers in France).&#xD;
      </textblock>
    </brief_summary>
    <detailed_description>
      <textblock>
        Thrombotic microangiopathies (TMAs) are a diverse, rare but serious group of diseases. Their&#xD;
        epidemiology has recently been elucidated thanks to work published by our team. It has been&#xD;
        shown that secondary TMAs account for 95% of cases, whereas primary TMAs (atypical hemolytic&#xD;
        syndromes (HUS) and thrombotic thrombocytopenic purpura (TTP)) account for only about 5%.&#xD;
  &#xD;
        However, many epidemiologic problems remain. First, many but not all patients with TMA as&#xD;
        classically defined (mechanical anemia, thrombocytopenia, elevated LDH, decreased&#xD;
        haptoglobin, schizocytes) have impaired renal function. If a renal biopsy is performed (which&#xD;
        is not always the case, as TMA is a risk factor for bleeding after renal biopsy), the renal&#xD;
        lesions do not always show &quot;renal-limited&quot; TMA. We also do not know which of the causes of&#xD;
        systemic TMA are associated with renal TMA and which are not.&#xD;
  &#xD;
        Conversely, in patients with renal biopsy, we can find stigmata of renal-limited TMA in the&#xD;
        absence of systemic TMA. Why do some patients have systemic TMA but not renal TMA and others&#xD;
        have renal TMA but not systemic TMA? Most studies are based on a few small clinical cases and&#xD;
        the literature reviews that report them.&#xD;
  &#xD;
        The vital, renal, and cardiovascular prognosis of patients with TMA obviously depends on the&#xD;
        cause, the clinical presentation of the patients, and their management. However, the renal,&#xD;
        systemic, and vital outcomes of renal-only vs. systemic-only vs. systemic and renal TMA,&#xD;
        regardless of the cause and severity of TMA, are currently unknown.&#xD;
  &#xD;
        As this is a rare disease, only a multicenter approach (&gt;20 centers) over a long period of&#xD;
        time (&gt;10 years), including highly recruited university and general hospitals, with&#xD;
        experienced and motivated investigators, can help us to answer these currently unanswered&#xD;
        questions (these investigators usually belong to the competence centers of the national&#xD;
        reference center).&#xD;
      </textblock>
    </detailed_description>
    <overall_status>Recruiting</overall_status>
    <start_date type="Actual">January 1, 2023</start_date>
    <completion_date type="Anticipated">January 2025</completion_date>
    <primary_completion_date type="Anticipated">January 2025</primary_completion_date>
    <study_type>Observational</study_type>
    <has_expanded_access>No</has_expanded_access>
    <study_design_info>
      <observational_model>Cohort</observational_model>
      <time_perspective>Retrospective</time_perspective>
    </study_design_info>
    <primary_outcome>
      <measure>Presence of isolated renal, hematological or renal associated with hematological features ot thrombotic microangiopathies</measure>
      <time_frame>1/ Baseline, ie date of kidney biopsy</time_frame>
      <description>Clinical data</description>
    </primary_outcome>
    <secondary_outcome>
      <measure>Assess correlations between specific anatomopathological lesions and thrombotic microangiopathies phenotypes</measure>
      <time_frame>1/ Baseline, ie date of kidney biopsy</time_frame>
      <description>Pathological and clinical data</description>
    </secondary_outcome>
    <secondary_outcome>
      <measure>Assess correlations between cause of thrombotic microangiopathies and clinical phenotypes</measure>
      <time_frame>1/ Baseline, ie date of kidney biopsy</time_frame>
      <description>Clinical data</description>
    </secondary_outcome>
    <secondary_outcome>
      <measure>Define the biological profile (standard biology and alternative complement pathway analyses including genetic data) of these thrombotic microangiopathies.</measure>
      <time_frame>1/ Up to 2 weeks after baseline date ; 2/ Date of last follow-up, an average of 2 years</time_frame>
      <description>Biological data</description>
    </secondary_outcome>
    <secondary_outcome>
      <measure>Define the renal, cardiovascular and vital prognosis of these patients</measure>
      <time_frame>1/ Hospital discharge date, an average of 2 weeks ; 2/ Date of last follow-up, an average of 2 years</time_frame>
      <description>Clinical data</description>
    </secondary_outcome>
    <secondary_outcome>
      <measure>Define treatments for these patients</measure>
      <time_frame>1/ Hospital discharge date, an average of 2 weeks</time_frame>
      <description>Clinical data</description>
    </secondary_outcome>
    <number_of_groups>1</number_of_groups>
    <enrollment type="Anticipated">1000</enrollment>
    <condition>Thrombotic Microangiopathy</condition>
    <condition>Acute Kidney Injury</condition>
    <condition>Hemolytic Uremic Syndrome</condition>
    <condition>Nephrology</condition>
    <condition>Kidney Diseases</condition>
    <arm_group>
      <arm_group_label>MATRIX</arm_group_label>
      <description>Thrombotic microangiopathy with kidney biopsy</description>
    </arm_group>
    <intervention>
      <intervention_type>Other</intervention_type>
      <intervention_name>Collecting datas</intervention_name>
      <description>Blood, Tissue and Urine samples</description>
      <arm_group_label>MATRIX</arm_group_label>
    </intervention>
    <biospec_retention>Samples With DNA</biospec_retention>
    <biospec_descr>
      <textblock>
        Blood, Tissue and Urine samples&#xD;
      </textblock>
    </biospec_descr>
    <eligibility>
      <study_pop>
        <textblock>
          The population corresponds to French adult nephrology patients with renal and/or systemic&#xD;
          thrombotic microangiopathy, for whom renal biopsy data are available. It is not extendable&#xD;
          to renal transplant patients.&#xD;
        </textblock>
      </study_pop>
      <sampling_method>Non-Probability Sample</sampling_method>
      <criteria>
        <textblock>
          Inclusion Criteria:&#xD;
  &#xD;
            1. Adult patients 18 years of age or older&#xD;
  &#xD;
            2. Who have undergone renal biopsy of the native kidney for impaired renal function&#xD;
               between 2009 and July 2022.&#xD;
  &#xD;
            3. Presence of classically defined systemic MAT (most of the following parameters:&#xD;
               elevated LDH, decreased haptoglobin, schizocytes, thrombocytopenia and anemia) AND/OR&#xD;
               presence of arteriolar or glomerular renal MAT as indicated by the pathologist&#xD;
               (including endothelial turgor, mesangiolysis, double contours, presence of thrombi,&#xD;
               fibrinoid necrosis of the arterial wall).&#xD;
  &#xD;
          Exclusion Criteria:&#xD;
  &#xD;
          1. Kidney transplantation&#xD;
        </textblock>
      </criteria>
      <gender>All</gender>
      <minimum_age>18 Years</minimum_age>
      <maximum_age>N/A</maximum_age>
      <healthy_volunteers>No</healthy_volunteers>
    </eligibility>
    <overall_official>
      <last_name>Jean-Michel Halimi, MD, PhD</last_name>
      <role>Study Director</role>
      <affiliation>CHRU TOURS, Nephrology</affiliation>
    </overall_official>
    <overall_official>
      <last_name>Valentin Maisons, MD</last_name>
      <role>Principal Investigator</role>
      <affiliation>CHRU TOURS, Nephrology</affiliation>
    </overall_official>
    <overall_contact>
      <last_name>Jean-Michel Halimi, MD, PhD</last_name>
      <phone>02.47.47.37.46</phone>
      <phone_ext>+33</phone_ext>
      <email>jmhalimi@univ-tours.fr</email>
    </overall_contact>
    <overall_contact_backup>
      <last_name>Valentin Maisons, MD</last_name>
      <phone>02.47.47.37.46</phone>
      <phone_ext>+33</phone_ext>
      <email>valentin.maisons@univ-tours.fr</email>
    </overall_contact_backup>
    <location>
      <facility>
        <name>Department of Nephrology, University Hospital of Tours</name>
        <address>
          <city>Tours</city>
          <zip>37044</zip>
          <country>France</country>
        </address>
      </facility>
      <status>Recruiting</status>
      <contact>
        <last_name>Jean-Michel Halimi, MD,PhD</last_name>
        <phone>02.47.47.37.46</phone>
        <phone_ext>+33</phone_ext>
        <email>jmhalimi@univ-tours.fr</email>
      </contact>
      <contact_backup>
        <last_name>Valentin Maisons, MD</last_name>
        <phone>02.47.47.37.46</phone>
        <phone_ext>+33</phone_ext>
        <email>valentin.maisons@univ-tours.fr</email>
      </contact_backup>
    </location>
    <location_countries>
      <country>France</country>
    </location_countries>
    <reference>
      <citation>Goodship TH, Cook HT, Fakhouri F, Fervenza FC, Fremeaux-Bacchi V, Kavanagh D, Nester CM, Noris M, Pickering MC, Rodriguez de Cordoba S, Roumenina LT, Sethi S, Smith RJ; Conference Participants. Atypical hemolytic uremic syndrome and C3 glomerulopathy: conclusions from a &quot;Kidney Disease: Improving Global Outcomes&quot; (KDIGO) Controversies Conference. Kidney Int. 2017 Mar;91(3):539-551. doi: 10.1016/j.kint.2016.10.005. Epub 2016 Dec 16.</citation>
      <PMID>27989322</PMID>
    </reference>
    <reference>
      <citation>Bayer G, von Tokarski F, Thoreau B, Bauvois A, Barbet C, Cloarec S, Merieau E, Lachot S, Garot D, Bernard L, Gyan E, Perrotin F, Pouplard C, Maillot F, Gatault P, Sautenet B, Rusch E, Buchler M, Vigneau C, Fakhouri F, Halimi JM. Etiology and Outcomes of Thrombotic Microangiopathies. Clin J Am Soc Nephrol. 2019 Apr 5;14(4):557-566. doi: 10.2215/CJN.11470918. Epub 2019 Mar 12.</citation>
      <PMID>30862697</PMID>
    </reference>
    <reference>
      <citation>Genest DS, Patriquin CJ, Licht C, John R, Reich HN. Renal Thrombotic Microangiopathy: A Review. Am J Kidney Dis. 2023 May;81(5):591-605. doi: 10.1053/j.ajkd.2022.10.014. Epub 2022 Dec 10.</citation>
      <PMID>36509342</PMID>
    </reference>
    <verification_date>August 2023</verification_date>
    <study_first_submitted>July 31, 2023</study_first_submitted>
    <study_first_submitted_qc>August 10, 2023</study_first_submitted_qc>
    <study_first_posted type="Actual">August 14, 2023</study_first_posted>
    <last_update_submitted>August 10, 2023</last_update_submitted>
    <last_update_submitted_qc>August 10, 2023</last_update_submitted_qc>
    <last_update_posted type="Actual">August 14, 2023</last_update_posted>
    <responsible_party>
      <responsible_party_type>Sponsor</responsible_party_type>
    </responsible_party>
    <keyword>Thrombotic microangiopathy</keyword>
    <keyword>Acute kidney injury</keyword>
    <keyword>Hemolytic uremic syndrome</keyword>
    <keyword>Kidney histology</keyword>
    <keyword>Complement</keyword>
    <condition_browse>
      <!-- CAUTION:  The following MeSH terms are assigned with an imperfect algorithm            -->
      <mesh_term>Kidney Diseases</mesh_term>
      <mesh_term>Acute Kidney Injury</mesh_term>
      <mesh_term>Hemolytic-Uremic Syndrome</mesh_term>
      <mesh_term>Vascular Diseases</mesh_term>
      <mesh_term>Thrombotic Microangiopathies</mesh_term>
      <mesh_term>Hemolysis</mesh_term>
    </condition_browse>
    <patient_data>
      <sharing_ipd>Undecided</sharing_ipd>
    </patient_data>
    <!-- Results have not yet been posted for this study                                          -->
  </clinical_study>
  
  
text: download date: ClinicalTrials.gov processed this data on September 20, 2023
  link text: Link to the current ClinicalTrials.gov record.
  url: https://clinicaltrials.gov/ct2/show/NCT05991245
  org study id: RNI/MATRIX
  secondary id: F20221110095846
  secondary id: 2022-59
  nct id: NCT05991245
  lead sponsor: 
  has dmc: No
  is fda regulated drug: No
  is fda regulated device: No
  Thrombotic microangiopathies (TMAs) are a diverse, rare but serious group of diseases.
        Progress has been made regarding the epidemiology of TMA (Bayer CJASN 2019). It has been
        shown that secondary TMAs account for 95% of cases, whereas primary TMAs (atypical hemolytic
        syndromes (HUS) and thrombotic thrombocytopenic purpura (TTP)) account for only about 5%.
  
        However, in many cases, the pathophysiology, optimal management and prognosis of TMA remains
        unclear and it has been shown that patients with TMA may have renal-limited TMA or renal and
        hematological TMA (ie. With (mechanical anemia, thrombocytopenia, elevated LDH, decreased
        haptoglobin, schistocytes). In most studies, kidney biopsies are not performed and the
        diagnostic workup is uncomplete.
  
        As this is a rare disease, only a multicenter approach (>20 centers) over a long period of
        time (>10 years), with adequate diagnostic workup including kidney biopsies can help us to
        answer these questions (investigators in the present are usually members of the CNR-MAT (a
        network of the TMA centers in France).
  Thrombotic microangiopathies (TMAs) are a diverse, rare but serious group of diseases. Their
        epidemiology has recently been elucidated thanks to work published by our team. It has been
        shown that secondary TMAs account for 95% of cases, whereas primary TMAs (atypical hemolytic
        syndromes (HUS) and thrombotic thrombocytopenic purpura (TTP)) account for only about 5%.
  
        However, many epidemiologic problems remain. First, many but not all patients with TMA as
        classically defined (mechanical anemia, thrombocytopenia, elevated LDH, decreased
        haptoglobin, schizocytes) have impaired renal function. If a renal biopsy is performed (which
        is not always the case, as TMA is a risk factor for bleeding after renal biopsy), the renal
        lesions do not always show "renal-limited" TMA. We also do not know which of the causes of
        systemic TMA are associated with renal TMA and which are not.
  
        Conversely, in patients with renal biopsy, we can find stigmata of renal-limited TMA in the
        absence of systemic TMA. Why do some patients have systemic TMA but not renal TMA and others
        have renal TMA but not systemic TMA? Most studies are based on a few small clinical cases and
        the literature reviews that report them.
  
        The vital, renal, and cardiovascular prognosis of patients with TMA obviously depends on the
        cause, the clinical presentation of the patients, and their management. However, the renal,
        systemic, and vital outcomes of renal-only vs. systemic-only vs. systemic and renal TMA,
        regardless of the cause and severity of TMA, are currently unknown.
  
        As this is a rare disease, only a multicenter approach (>20 centers) over a long period of
        time (>10 years), including highly recruited university and general hospitals, with
        experienced and motivated investigators, can help us to answer these currently unanswered
        questions (these investigators usually belong to the competence centers of the national
        reference center).
  observational model: Cohort
  time perspective: Retrospective
  measure: Presence of isolated renal, hematological or renal associated with hematological features ot thrombotic microangiopathies
  time frame: 1/ Baseline, ie date of kidney biopsy
  description: Clinical data
  measure: Assess correlations between specific anatomopathological lesions and thrombotic microangiopathies phenotypes
  time frame: 1/ Baseline, ie date of kidney biopsy
  description: Pathological and clinical data
  measure: Assess correlations between cause of thrombotic microangiopathies and clinical phenotypes
  time frame: 1/ Baseline, ie date of kidney biopsy
  description: Clinical data
  measure: Define the biological profile (standard biology and alternative complement pathway analyses including genetic data) of these thrombotic microangiopathies.
  time frame: 1/ Up to 2 weeks after baseline date ; 2/ Date of last follow-up, an average of 2 years
  description: Biological data
  measure: Define the renal, cardiovascular and vital prognosis of these patients
  time frame: 1/ Hospital discharge date, an average of 2 weeks ; 2/ Date of last follow-up, an average of 2 years
  description: Clinical data
  measure: Define treatments for these patients
  time frame: 1/ Hospital discharge date, an average of 2 weeks
  description: Clinical data
  arm group label: MATRIX
  description: Thrombotic microangiopathy with kidney biopsy
  intervention type: Other
  intervention name: Collecting datas
  description: Blood, Tissue and Urine samples
  arm group label: MATRIX
  Blood, Tissue and Urine samples
  study pop: 
  sampling method: Non-Probability Sample
  criteria: 
  gender: All
  minimum age: 18 Years
  maximum age: N/A
  healthy volunteers: No
  last name: Jean-Michel Halimi, MD, PhD
  role: Study Director
  affiliation: CHRU TOURS, Nephrology
  last name: Valentin Maisons, MD
  role: Principal Investigator
  affiliation: CHRU TOURS, Nephrology
  last name: Jean-Michel Halimi, MD, PhD
  phone: 02.47.47.37.46
  phone ext: +33
  email: jmhalimi@univ-tours.fr
  last name: Valentin Maisons, MD
  phone: 02.47.47.37.46
  phone ext: +33
  email: valentin.maisons@univ-tours.fr
  facility: 
  status: Recruiting
  contact: 
  contact backup: 
  country: France
  citation: Goodship TH, Cook HT, Fakhouri F, Fervenza FC, Fremeaux-Bacchi V, Kavanagh D, Nester CM, Noris M, Pickering MC, Rodriguez de Cordoba S, Roumenina LT, Sethi S, Smith RJ; Conference Participants. Atypical hemolytic uremic syndrome and C3 glomerulopathy: conclusions from a "Kidney Disease: Improving Global Outcomes" (KDIGO) Controversies Conference. Kidney Int. 2017 Mar;91(3):539-551. doi: 10.1016/j.kint.2016.10.005. Epub 2016 Dec 16.
  PMID: 27989322
  citation: Bayer G, von Tokarski F, Thoreau B, Bauvois A, Barbet C, Cloarec S, Merieau E, Lachot S, Garot D, Bernard L, Gyan E, Perrotin F, Pouplard C, Maillot F, Gatault P, Sautenet B, Rusch E, Buchler M, Vigneau C, Fakhouri F, Halimi JM. Etiology and Outcomes of Thrombotic Microangiopathies. Clin J Am Soc Nephrol. 2019 Apr 5;14(4):557-566. doi: 10.2215/CJN.11470918. Epub 2019 Mar 12.
  PMID: 30862697
  citation: Genest DS, Patriquin CJ, Licht C, John R, Reich HN. Renal Thrombotic Microangiopathy: A Review. Am J Kidney Dis. 2023 May;81(5):591-605. doi: 10.1053/j.ajkd.2022.10.014. Epub 2022 Dec 10.
  PMID: 36509342
  responsible party type: Sponsor
  mesh term: Kidney Diseases
  mesh term: Acute Kidney Injury
  mesh term: Hemolytic-Uremic Syndrome
  mesh term: Vascular Diseases
  mesh term: Thrombotic Microangiopathies
  mesh term: Hemolysis
  sharing ipd: Undecided