Hemolytic-Uremic SyndromeCOMPRareNCT05985122
New Analytic Tools for aHUS and C3G Diagnosis
A study testing C3NEF assay in people with Hemolytic-Uremic Syndrome and Membranoproliferative Glomerulonephritis, run by Mario Negri Institute for Pharmacological Research at 1 site in Italy.
Trial summary
This protocol is part of a larger project, COMPRare (COMPlement-mediated Rare kidney diseases), which has been financed on behalf of the EJP RD (European Joint Programme on Rare Diseases) program of EU and is leaded by a scientific consortium from 7 European countries. The partners (P) of the consortium are: P1. Read more about this study
- Who is it for?
- Any ageHealthy volunteers can take part
- Conditions the study is for
- Hemolytic-Uremic Syndrome, Membranoproliferative Glomerulonephritis, Healthy
- What is being tested?
- C3NEF assay
- Could I receive a placebo?
- No, everyone receives an active treatment
- How many people
- 180 participants
- Where
- 1 siteItaly
- Study dates
- 1 Jul 2023to Oct 2026
- Phase
- Interventional
- Are there results?
- Not yet: the study is under way
Key requirements
Who can take part, as listed by the sponsor. Only the study team can confirm whether you are eligible, so take this list to your doctor.
- Ages Any age
- All sexes
- Healthy volunteers accepted
- Child, Adult, Older adult
Who may be able to join
- Male and female patients (children and adults) with C3G diagnosis
- Biobank written informed consent
- Aim 2 Inclusion criteria
- Male and female patients (children and adults) with aHUS diagnosis in acute phase (before any treatment), or in remission either untreated or undergoing anti-C5 treatment at standard dosing
- Written informed consent Exclusion criteria
- Stx-associated HUS
- TTP (ADAMTS13<10%)
- Plasma therapy within 2 weeks from blood sampling
Who cannot join
None listed.
Trial locations and contacts
1 site in 1 country.
Italy1 site
Centro di Ricerche Cliniche per le Malattie Rare "Aldo e Cele Daccò"
Ranica, BG, 24020
About this study
Official title: Towards the Most Accurate Diagnosis and Monitoring of Complement-mediated Rare Kidney Diseases
This protocol is part of a larger project, COMPRare (COMPlement-mediated Rare kidney diseases), which has been financed on behalf of the EJP RD (European Joint Programme on Rare Diseases) program of EU and is leaded by a scientific consortium from 7 European countries.
The partners (P) of the consortium are:
Read more
P1. Radboudumc Amalia Children's Hospital (The Netherlands) P2. Semmelweis University (Hungary) P3. Cordeliers Research Center (France) P4. Max Delbruck Center for Molecular Medicine (Germany) P5. Istituto di Ricerche Farmacologiche Mario Negri (Italy) P6. Lund University (Sweden) P7. Lille University (France)
The general aim of the project is to define new diagnostic tools for complement activation in order to improve patients stratification and follow-up, thereby affecting time and choice of treatment in patients with aHUS and C3G.
Particularly, the specific objectives of the COMPRare are:
- To develop new standardized analytic assays thereby identifying specific complement prognostic biomarkers for early diagnosis, classification, improved monitoring and treatment of patients with aHUS and C3G;
- To in-depth characterize patients' complement abnormalities in blood, in patient-derived cells and in kidney biopsies;
- To identify strategies to classify VUS/LPV
- To find new pathophysiological pathways involved in aHUS and C3G for further improving disease diagnosis, monitoring and treatment.
The results of these studies will form the basis of personalized treatment with existing and upcoming complement inhibitory drugs for these rare complement-mediated kidney diseases.
Read the detailed description
Atypical Hemolytic Uremic Syndrome (aHUS) and C3 Glomerulopathies (C3G) are ultra-rare conditions in which an uncontrolled complement activation results in renal inflammation with thrombotic microangiopathy (TMA) in aHUS and extensive deposition of complement fragments in the kidneys in C3G. In both conditions, these alterations lead to acute and chronic kidney damage and, ultimately, end-stage renal failure. The prevalence of genetic and acquired complement abnormalities varies between the two diseases, but covers mostly the same complement proteins. Blocking the complement system is the treatment of choice in aHUS and may have considerable potential in C3G, as evident from the increasing number of phase 3 trials with complement inhibitory drugs. Timely and accurate diagnosis is still challenging for clinicians, both for aHUS, to differentiate it from other forms of TMA, and for C3G, to distinguish it from other forms of glomerulonephritis (GN). In C3G, kidney biopsy is the diagnostic gold standard but it is not sufficient. Therefore, for both aHUS and C3G, there is an unmet need for accurate testing of genetic and acquired complement abnormalities. Moreover, interlaboratory complement-assays, in particular the tests for the C3 Nephritic Factors (C3NeFs; heterogeneous autoantibodies that stabilize the C3 convertase), vary considerably and, consequently, their standardization is a great necessity. Furthermore, the interpretation of genetic results in aHUS and C3G is not always conclusive.
Variants of Unknown Significance (VUS)/Likely Pathogenic Variant (LPV) in complement genes are often found in aHUS and C3G and require further characterization. A rapid and functional VUS/LPV determination and interpretation could help to better understand the disease pathophysiology and might influence diagnosis and treatment options.
Currently, aHUS patients are effectively treated with the complement C5 inhibiting monoclonal antibodies Eculizumab and Ravulizumab. However, the duration and optimal dose of treatment are debated, particularly in view of the high costs of the drug. Even if recent studies showed that restrictive use of eculizumab is feasible, there is a clear need for biomarkers identification and protocols for monitoring and predicting disease activity in aHUS and C3G patients.
In summary, new analytic tools for further defining the disease profile in blood, (patients) cells and kidney biopsies are needed.
- Being tested
- C3NEF assay
- Keywords
- Complement-mediated kidney diseases, Blood and tissue biomarkers, Assay standardization, Glycocalyx, Characterization of variants of unknown significance
- Medical subject headings
- Hemolytic-Uremic Syndrome, Glomerulonephritis, Membranoproliferative
What participants receive
What participants receive. In a randomised study each person is assigned to one group by chance.
C3NEF assayDiagnostic test
This assay will consist of a dual test, detecting C3 convertase binding C3NEF autoantibodies and measuring the functional consequence by complement alternative pathway (AP) activity using two distinct ELISA designs: C3NEF detection assay and AP activity assay.
| Study group | Role | What they receive |
|---|---|---|
| Patients | Experimental | Patients diagnosed with C3G (15 positive and 15 negative for C3NEF) at Centro Daccò, will be identified between those who provided consent to store their samples in the certified biobank (UNI EN ISO 9001:2015; certification n° 6121) of "Centro Daccò" (Centro di Risorse Biologiche Mario Negri - Biobanca Malattie Rare e Renali) and to share them with external laboratories. Receives: Diagnostic Test: C3NEF assay |
| Healthy controls | Active comparator | Healthy donors will be identified between those who provided consent to store their samples in the certified biobank (UNI EN ISO 9001:2015; certification n° 6121) of "Centro Daccò" (Centro di Risorse Biologiche Mario Negri - Biobanca Malattie Rare e Renali). Subject that meet the inclusion/exclusion criteria and for which there is no enough material stored in our biobank, will be recontacted by the investigators of "Centro Daccò" and, if agree, will be asked for serum sampling after informed consent signature. Receives: Diagnostic Test: C3NEF assay |
What is being measured
The primary outcome is the main question the study is designed to answer.
Determination of assay sensitivity and specificity
We estimate that 38 VUS/LPV carrying pedigrees should be enough to demonstrate the sensitivity and specificity of the assay for classifying VUS/LPV.
Measured: At day 0
Timeline
From the start of the study to its completion; the mark is today. Estimated dates are the sponsor’s plan.
- First posted14 Aug 2023
- Study start1 Jul 2023
- Primary completionOct 2026 (estimated)
- Study completionOct 2026 (estimated)
Resources
- Official record on ClinicalTrials.govThe registry entry this page is built from, with its full change history.
- Publications (8)Papers the sponsor has linked to this study.
- Other trials for Hemolytic-Uremic SyndromeStudies of the same condition, open and under way.
- More trials run by Mario Negri Institute for Pharmacological ResearchThe sponsor's other registered studies.
- What the trial phases meanHow a treatment moves from first tests in people to approval.
More details
For doctors and researchers: how the study is designed, who runs it, and its registry IDs.
Study design
- Study type
- Interventional
- Phase
- Phase N/A
- Primary purpose
- Diagnosis
- Allocation
- Non-randomised
- Intervention model
- Parallel groups
- Model description
- The samples (healthy volunteers and HUS or MPGN patients) for the study will be identified between those of patients and healthy controls who provided consent to store their samples in the certified biobank of "Centro Daccò" (Centro di Risorse Biologiche Mario Negri - Biobanca Malattie Rare e Renali) for two previousely approved studies.
- Masking
- None (open label)
- Enrolment
- 180 participants (estimated)
Sponsor and investigators
- Sponsor type
- University, hospital or other
- Responsible party
- Sponsor
- Investigators
- Marina Noris, PhD, Principal investigator, Istituto Di Ricerche Farmacologiche Mario Negri
IDs, dates and publications
- ClinicalTrials.gov ID
- NCT05985122
- Sponsor's protocol ID
- COMPRare-IRFMN
- Acronym
- COMPRare
- Status last verified
- Mar 2026
- First submitted
- 2 Aug 2023
- Last updated
- 23 Mar 2026
- Results posted
- No
- Data monitoring committee
- No
- FDA-regulated drug
- No
- FDA-regulated device
- No
- Individual data sharing
- No
Publications
Noris M, Galbusera M, Gastoldi S, Macor P, Banterla F, Bresin E, Tripodo C, Bettoni S, Donadelli R, Valoti E, Tedesco F, Amore A, Coppo R, Ruggenenti P, Gotti E, Remuzzi G. Dynamics of complement activation in aHUS and how to monitor eculizumab therapy. Blood. 2014 Sep 11;124(11):1715-26. doi: 10.1182/blood-2014-02-558296. Epub 2014 Jul 18.
PubMed 25037630Iatropoulos P, Daina E, Curreri M, Piras R, Valoti E, Mele C, Bresin E, Gamba S, Alberti M, Breno M, Perna A, Bettoni S, Sabadini E, Murer L, Vivarelli M, Noris M, Remuzzi G; Registry of Membranoproliferative Glomerulonephritis/C3 Glomerulopathy; Nastasi. Cluster Analysis Identifies Distinct Pathogenetic Patterns in C3 Glomerulopathies/Immune Complex-Mediated Membranoproliferative GN. J Am Soc Nephrol. 2018 Jan;29(1):283-294. doi: 10.1681/ASN.2017030258. Epub 2017 Oct 13.
PubMed 29030465Donadelli R, Pulieri P, Piras R, Iatropoulos P, Valoti E, Benigni A, Remuzzi G, Noris M. Unraveling the Molecular Mechanisms Underlying Complement Dysregulation by Nephritic Factors in C3G and IC-MPGN. Front Immunol. 2018 Oct 15;9:2329. doi: 10.3389/fimmu.2018.02329. eCollection 2018.
PubMed 30487789Galbusera M, Noris M, Gastoldi S, Bresin E, Mele C, Breno M, Cuccarolo P, Alberti M, Valoti E, Piras R, Donadelli R, Vivarelli M, Murer L, Pecoraro C, Ferrari E, Perna A, Benigni A, Portalupi V, Remuzzi G. An Ex Vivo Test of Complement Activation on Endothelium for Individualized Eculizumab Therapy in Hemolytic Uremic Syndrome. Am J Kidney Dis. 2019 Jul;74(1):56-72. doi: 10.1053/j.ajkd.2018.11.012. Epub 2019 Mar 7.
PubMed 30851964Piras R, Breno M, Valoti E, Alberti M, Iatropoulos P, Mele C, Bresin E, Donadelli R, Cuccarolo P, Smith RJH, Benigni A, Remuzzi G, Noris M. CFH and CFHR Copy Number Variations in C3 Glomerulopathy and Immune Complex-Mediated Membranoproliferative Glomerulonephritis. Front Genet. 2021 Jun 11;12:670727. doi: 10.3389/fgene.2021.670727. eCollection 2021.
PubMed 34211499Aiello S, Gastoldi S, Galbusera M, Ruggenenti P, Portalupi V, Rota S, Rubis N, Liguori L, Conti S, Tironi M, Gamba S, Santarsiero D, Benigni A, Remuzzi G, Noris M. C5a and C5aR1 are key drivers of microvascular platelet aggregation in clinical entities spanning from aHUS to COVID-19. Blood Adv. 2022 Jan 8;6(3):866-881. doi: 10.1182/bloodadvances.2021005246.
PubMed 34852172Piras R, Valoti E, Alberti M, Bresin E, Mele C, Breno M, Liguori L, Donadelli R, Rigoldi M, Benigni A, Remuzzi G, Noris M. CFH and CFHR structural variants in atypical Hemolytic Uremic Syndrome: Prevalence, genomic characterization and impact on outcome. Front Immunol. 2023 Jan 30;13:1011580. doi: 10.3389/fimmu.2022.1011580. eCollection 2022.
PubMed 36793547Gastoldi S, Aiello S, Galbusera M, Breno M, Alberti M, Bresin E, Mele C, Piras R, Liguori L, Santarsiero D, Benigni A, Remuzzi G, Noris M. An ex vivo test to investigate genetic factors conferring susceptibility to atypical haemolytic uremic syndrome. Front Immunol. 2023 Feb 9;14:1112257. doi: 10.3389/fimmu.2023.1112257. eCollection 2023.
PubMed 36845135
Study at a glance
From the registry record, last updated by the sponsor on 23 Mar 2026. Recruitment status is as the sponsor reported it: confirm with the study team.
- Official title
- Towards the Most Accurate Diagnosis and Monitoring of Complement-mediated Rare Kidney Diseases
- ClinicalTrials.gov ID
- NCT05985122
- Acronym / sponsor ID
- COMPRare / COMPRare-IRFMN
- Keywords
- Complement-mediated kidney diseases, Blood and tissue biomarkers, Assay standardization, Glycocalyx, Characterization of variants of unknown significance
- Study type
- Interventional
- Recruitment status
- Active, not recruiting
- Enrolment
- 180 participants (estimated)
- Lead sponsor
- Mario Negri Institute for Pharmacological ResearchUniversity, hospital or other
- Study start
- 1 Jul 2023 (actual)
- Primary completion
- Oct 2026 (estimated)
- Study completion
- Oct 2026 (estimated)
- First posted
- 14 Aug 2023 (actual)
- Results
- Not posted in the source record
Clinical summary
The research question as the sponsor registered it. This describes what the study plans to test, not what it found.
This protocol is part of a larger project, COMPRare (COMPlement-mediated Rare kidney diseases), which has been financed on behalf of the EJP RD (European Joint Programme on Rare Diseases) program of EU and is leaded by a scientific consortium from 7 European countries.
The partners (P) of the consortium are:
P1. Radboudumc Amalia Children's Hospital (The Netherlands) P2. Semmelweis University (Hungary) P3. Cordeliers Research Center (France) P4. Max Delbruck Center for Molecular Medicine (Germany) P5. Istituto di Ricerche Farmacologiche Mario Negri (Italy) P6. Lund University (Sweden) P7. Lille University (France)
The general aim of the project is to define new diagnostic tools for complement activation in order to improve patients stratification and follow-up, thereby affecting time and choice of treatment in patients with aHUS and C3G.
Particularly, the specific objectives of the COMPRare are:
- To develop new standardized analytic assays thereby identifying specific complement prognostic biomarkers for early diagnosis, classification, improved monitoring and treatment of patients with aHUS and C3G;
- To in-depth characterize patients' complement abnormalities in blood, in patient-derived cells and in kidney biopsies;
- To identify strategies to classify VUS/LPV
- To find new pathophysiological pathways involved in aHUS and C3G for further improving disease diagnosis, monitoring and treatment.
The results of these studies will form the basis of personalized treatment with existing and upcoming complement inhibitory drugs for these rare complement-mediated kidney diseases.
Detailed description
Atypical Hemolytic Uremic Syndrome (aHUS) and C3 Glomerulopathies (C3G) are ultra-rare conditions in which an uncontrolled complement activation results in renal inflammation with thrombotic microangiopathy (TMA) in aHUS and extensive deposition of complement fragments in the kidneys in C3G. In both conditions, these alterations lead to acute and chronic kidney damage and, ultimately, end-stage renal failure. The prevalence of genetic and acquired complement abnormalities varies between the two diseases, but covers mostly the same complement proteins. Blocking the complement system is the treatment of choice in aHUS and may have considerable potential in C3G, as evident from the increasing number of phase 3 trials with complement inhibitory drugs. Timely and accurate diagnosis is still challenging for clinicians, both for aHUS, to differentiate it from other forms of TMA, and for C3G, to distinguish it from other forms of glomerulonephritis (GN). In C3G, kidney biopsy is the diagnostic gold standard but it is not sufficient. Therefore, for both aHUS and C3G, there is an unmet need for accurate testing of genetic and acquired complement abnormalities. Moreover, interlaboratory complement-assays, in particular the tests for the C3 Nephritic Factors (C3NeFs; heterogeneous autoantibodies that stabilize the C3 convertase), vary considerably and, consequently, their standardization is a great necessity. Furthermore, the interpretation of genetic results in aHUS and C3G is not always conclusive.
Variants of Unknown Significance (VUS)/Likely Pathogenic Variant (LPV) in complement genes are often found in aHUS and C3G and require further characterization. A rapid and functional VUS/LPV determination and interpretation could help to better understand the disease pathophysiology and might influence diagnosis and treatment options.
Currently, aHUS patients are effectively treated with the complement C5 inhibiting monoclonal antibodies Eculizumab and Ravulizumab. However, the duration and optimal dose of treatment are debated, particularly in view of the high costs of the drug. Even if recent studies showed that restrictive use of eculizumab is feasible, there is a clear need for biomarkers identification and protocols for monitoring and predicting disease activity in aHUS and C3G patients.
In summary, new analytic tools for further defining the disease profile in blood, (patients) cells and kidney biopsies are needed.
Study design
- Primary purpose
- Diagnosis
- Allocation
- Non-randomised
- Intervention model
- Parallel groups
- Masking
- None (open label)
- Number of arms
- 2
- Model description
- The samples (healthy volunteers and HUS or MPGN patients) for the study will be identified between those of patients and healthy controls who provided consent to store their samples in the certified biobank of "Centro Daccò" (Centro di Risorse Biologiche Mario Negri - Biobanca Malattie Rare e Renali) for two previousely approved studies.
| Arm | Type | Receives |
|---|---|---|
| Patients | Experimental | Diagnostic Test: C3NEF assayPatients diagnosed with C3G (15 positive and 15 negative for C3NEF) at Centro Daccò, will be identified between those who provided consent to store their samples in the certified biobank (UNI EN ISO 9001:2015; certification n° 6121) of "Centro Daccò" (Centro di Risorse Biologiche Mario Negri - Biobanca Malattie Rare e Renali) and to share them with external laboratories. |
| Healthy controls | Active comparator | Diagnostic Test: C3NEF assayHealthy donors will be identified between those who provided consent to store their samples in the certified biobank (UNI EN ISO 9001:2015; certification n° 6121) of "Centro Daccò" (Centro di Risorse Biologiche Mario Negri - Biobanca Malattie Rare e Renali). Subject that meet the inclusion/exclusion criteria and for which there is no enough material stored in our biobank, will be recontacted by the investigators of "Centro Daccò" and, if agree, will be asked for serum sampling after informed consent signature. |
Who may qualify
- Sex
- All
- Healthy volunteers
- Accepted
- Age groups
- Child, Adult, Older adult
Key inclusion criteria (8 listed)
- Male and female patients (children and adults) with C3G diagnosis
- Biobank written informed consent
- Aim 2 Inclusion criteria
- Male and female patients (children and adults) with aHUS diagnosis in acute phase (before any treatment), or in remission either untreated or undergoing anti-C5 treatment at standard dosing
- Written informed consent Exclusion criteria
Key exclusion criteria (0 listed)
Eligibility is decided by the study team after screening; this overview does not establish that a patient qualifies. Full inclusion and exclusion criteria.
Interventions
| Intervention | Type | Arms |
|---|---|---|
| C3NEF assayThis assay will consist of a dual test, detecting C3 convertase binding C3NEF autoantibodies and measuring the functional consequence by complement alternative pathway (AP) activity using two distinct ELISA designs: C3NEF detection assay and AP activity assay. | Diagnostic test | Healthy controls, Patients |
Primary outcome
Determination of assay sensitivity and specificity
Time frame: At day 0
We estimate that 38 VUS/LPV carrying pedigrees should be enough to demonstrate the sensitivity and specificity of the assay for classifying VUS/LPV.
Results and safety
This study is still under way. Results are not available in the source record yet.
Research links
- Official record on ClinicalTrials.govLast updated by the sponsor 23 Mar 2026.
- Background: PubMed 25037630Noris M, Galbusera M, Gastoldi S, Macor P, Banterla F, Bresin E, Tripodo C, Bettoni S, Donadelli R, Valoti E, Tedesco F, Amore A, Coppo R, Ruggenenti P, Gotti E, Remuzzi G. Dynamics of complement activation in aHUS and how to monitor eculizumab therapy. Blood. 2014 Sep 11;124(11):1715-26. doi: 10.1182/blood-2014-02-558296. Epub 2014 Jul 18.
- Background: PubMed 29030465Iatropoulos P, Daina E, Curreri M, Piras R, Valoti E, Mele C, Bresin E, Gamba S, Alberti M, Breno M, Perna A, Bettoni S, Sabadini E, Murer L, Vivarelli M, Noris M, Remuzzi G; Registry of Membranoproliferative Glomerulonephritis/C3 Glomerulopathy; Nastasi. Cluster Analysis Identifies Distinct Pathogenetic Patterns in C3 Glomerulopathies/Immune Complex-Mediated Membranoproliferative GN. J Am Soc Nephrol. 2018 Jan;29(1):283-294. doi: 10.1681/ASN.2017030258. Epub 2017 Oct 13.
- Background: PubMed 30487789Donadelli R, Pulieri P, Piras R, Iatropoulos P, Valoti E, Benigni A, Remuzzi G, Noris M. Unraveling the Molecular Mechanisms Underlying Complement Dysregulation by Nephritic Factors in C3G and IC-MPGN. Front Immunol. 2018 Oct 15;9:2329. doi: 10.3389/fimmu.2018.02329. eCollection 2018.
- Background: PubMed 30851964Galbusera M, Noris M, Gastoldi S, Bresin E, Mele C, Breno M, Cuccarolo P, Alberti M, Valoti E, Piras R, Donadelli R, Vivarelli M, Murer L, Pecoraro C, Ferrari E, Perna A, Benigni A, Portalupi V, Remuzzi G. An Ex Vivo Test of Complement Activation on Endothelium for Individualized Eculizumab Therapy in Hemolytic Uremic Syndrome. Am J Kidney Dis. 2019 Jul;74(1):56-72. doi: 10.1053/j.ajkd.2018.11.012. Epub 2019 Mar 7.
- Background: PubMed 34211499Piras R, Breno M, Valoti E, Alberti M, Iatropoulos P, Mele C, Bresin E, Donadelli R, Cuccarolo P, Smith RJH, Benigni A, Remuzzi G, Noris M. CFH and CFHR Copy Number Variations in C3 Glomerulopathy and Immune Complex-Mediated Membranoproliferative Glomerulonephritis. Front Genet. 2021 Jun 11;12:670727. doi: 10.3389/fgene.2021.670727. eCollection 2021.
- Background: PubMed 34852172Aiello S, Gastoldi S, Galbusera M, Ruggenenti P, Portalupi V, Rota S, Rubis N, Liguori L, Conti S, Tironi M, Gamba S, Santarsiero D, Benigni A, Remuzzi G, Noris M. C5a and C5aR1 are key drivers of microvascular platelet aggregation in clinical entities spanning from aHUS to COVID-19. Blood Adv. 2022 Jan 8;6(3):866-881. doi: 10.1182/bloodadvances.2021005246.
- Background: PubMed 36793547Piras R, Valoti E, Alberti M, Bresin E, Mele C, Breno M, Liguori L, Donadelli R, Rigoldi M, Benigni A, Remuzzi G, Noris M. CFH and CFHR structural variants in atypical Hemolytic Uremic Syndrome: Prevalence, genomic characterization and impact on outcome. Front Immunol. 2023 Jan 30;13:1011580. doi: 10.3389/fimmu.2022.1011580. eCollection 2022.
- Background: PubMed 36845135Gastoldi S, Aiello S, Galbusera M, Breno M, Alberti M, Bresin E, Mele C, Piras R, Liguori L, Santarsiero D, Benigni A, Remuzzi G, Noris M. An ex vivo test to investigate genetic factors conferring susceptibility to atypical haemolytic uremic syndrome. Front Immunol. 2023 Feb 9;14:1112257. doi: 10.3389/fimmu.2023.1112257. eCollection 2023.
- Individual participant dataSharing planned: No
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Referral and contact
AzTrials does not enrol participants or take referrals. Contact the study team or a site listed below; they decide who can take part. This study is not recruiting at the moment.
Marina Noris, PhD principal investigator
Istituto Di Ricerche Farmacologiche Mario Negri
1 site in 1 country: see every site and its status.
Questions about this trial
What is this clinical trial studying?
A study testing C3NEF assay in people with Hemolytic-Uremic Syndrome and Membranoproliferative Glomerulonephritis, run by Mario Negri Institute for Pharmacological Research at 1 site in Italy.
The full registered description is in the About this study section and the official record.
Who may be eligible to take part?
The sponsor lists 8 inclusion and 0 exclusion criteria. Eligibility is decided by the study team after screening, so read the full criteria and contact a listed site.
Is this clinical trial currently recruiting?
The record says: under way, not looking for participants, as of the sponsor's last update on 23 Mar 2026. Status can change between updates, so confirm with the study contact before making plans.
Where is the study taking place?
The record lists 1 site in Italy. Whether a site is taking part right now should be confirmed with that site. See every site.
What are the possible benefits and risks?
They depend on the study and the treatment, and no study can promise a benefit. The study team explains the known risks during informed consent, before anyone joins; the record itself does not list them.
Are results available for this study?
This study is still under way. Results are not available in the source record yet.
How can a doctor refer a patient or contact the research team?
The record lists no contact. The official record names the sponsor, who can be asked directly. AzTrials does not enrol participants or take referrals.
What does the primary outcome measure?
Determination of assay sensitivity and specificity (time frame: At day 0). It is what the study was designed to measure, not a finding.
Where can I read the original study information?
On the ClinicalTrials.gov record for NCT05985122, which also lists 8 linked publications.
Does a listing mean the treatment is approved or proven to work?
No. A listing means the study is registered. It does not show that the treatment is safe, works, or is approved by a regulator.
How often is this information updated?
AzTrials copies changed records from ClinicalTrials.gov every night and reloads the whole registry every week. The sponsor last updated this record on 23 Mar 2026.