DiabetesKID-CODENCT07292493
Immune System in Diabetic Kidney Disease
An observational study of Diabetes and Diabetic Kidney Disease, run by University Medical Centre Ljubljana at 1 site in Slovenia.
Trial summary
Diabetes is a chronic condition marked by long-term elevated blood glucose levels. There are more types of diabetes; the majority of patients have type 1 or type 2 diabetes. Over long period of time, high blood sugar damages blood vessels and organs. Read more about this study
- Who is it for?
- Ages 40 to 65 years
- Conditions the study is for
- Diabetes, Diabetic Kidney Disease, Complement System
- How many people
- 90 participants
- Where
- 1 siteSlovenia
- Study dates
- 1 Dec 2025to Dec 2028
- Phase
- Observational
- 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 40 to 65 years
- All sexes
- No healthy volunteers
- Adult, Older adult
Study population: Patients with type 1 and type 2 diabetes, who are being treated at the diabetology outpatient clinic of the Department of Endocrinology, Diabetes, and Metabolic Diseases, University Medical Centre Ljubljana.
Who may be able to join
- body mass index below 30 kg/m²
- unknown macrovascular complications
- treated with angiotensin-converting enzyme inhibitors or angiotensin receptor blockers at the highest tolerated dose
Who cannot join
- a body mass index above 30 kg/m²
- macrovascular complications
Trial locations and contacts
1 site in 1 country. Contact the study team or a site near you to ask about taking part.
About this study
Official title: The Role of Complement in Diabetic Kidney Disease
Diabetes is a chronic condition marked by long-term elevated blood glucose levels. There are more types of diabetes; the majority of patients have type 1 or type 2 diabetes. Over long period of time, high blood sugar damages blood vessels and organs. One of the most common complications is diabetic kidney disease, which can slowly lead to kidney failure. People with this condition also have a much higher risk of heart and blood vessel diseases.
Newer research shows that the immune system, especially the complement system (a group of proteins that help defend the body), may also play a role in worsening kidney disease in diabetes. High blood sugar can activate these proteins, and they have been found in kidney tissue of patients with diabetic kidney disease.
The goal of this study is to find out how much the complement system contributes to kidney damage in diabetes, whether it affects different groups of patients differently, and whether it is linked to blood vessel health or the stage of kidney disease. The study will also assess if improved diabetes control is linked to reduced complement system activity.
Read the detailed description
Diabetes is a chronic disease characterized by long-term elevated blood glucose levels. Several types of diabetes are known, with most affected individuals having type 1 or type 2 diabetes. Long-term elevation of blood glucose affects various organs in the body, a condition referred to as chronic complications of diabetes. Since elevated blood glucose damages both small and large blood vessels, complications are classified as microvascular (damage to small vessels) and macrovascular (damage to large vessels). Diabetic kidney disease is the main microvascular complication in both type 1 and type 2 diabetes and is also the leading cause of kidney failure.
Changes in the kidneys develop over many years. Gradual deterioration of kidney function is monitored using laboratory parameters. Along with declining kidney function, blood pressure also increases, and cardiovascular diseases begin to develop- the risk of these rises exponentially with worsening kidney function. Cardiovascular diseases represent the leading cause of mortality among people with diabetes.
Traditionally, diabetic kidney disease was considered as non-inflammatory condition. Its development was attributed to impaired glucose metabolism and elevated blood pressure. Consequently, achieving optimal blood glucose and blood pressure values has been regarded as key to preventing chronic complications. However, diabetes itself represents an additional risk factor for cardiovascular disease compared with individuals without diabetes. Thus, individuals with diabetic kidney disease are even more prone to cardiovascular events. In these patients it is especially important to follow treatment guidelines and to treat elevated blood glucose and blood pressure as intensively as possible. For individuals with diabetic kidney disease, medications from the group of angiotensin-converting enzyme inhibitors or angiotensin receptor blockers are prescribed for the treatment of high blood pressure. Both medication groups also have a protective effect on the kidneys and slow the decline of kidney function. Angiotensin is a substance in the body responsible for raising blood pressure-when its action is inhibited, blood pressure decreases.
The investigators now know that inflammation and the immune system also play a role in the development of chronic diabetic complications. The complement system (a group of proteins in the blood involved in immune responses) is becoming recognized for its importance. Current studies do not suggest that the complement system plays a key role in the onset of the disease; however, its role in the progression of diabetic kidney disease and possibly in the occurrence of different forms of the disease has become evident. Hyperglycaemia increases the activity of certain complement proteins and activates specific pathways, while the hyperglycaemic environment also impairs the regulation of some proteins. Kidney biopsies of individuals with diabetic kidney disease have shown the presence of complement proteins in kidney tissue, and gene expression analyses have identified activation of complement-related genes.
The purpose of this study is to determine whether and to what extent activation of the complement system contributes to diabetic kidney disease and to define potential differences among different groups of individuals with diabetes. Additionally, the investigators aim to determine whether there is a connection between complement system activation and arterial function, as well as between complement system activation and the stage of kidney disease. The investigators will also investigate whether diabetes control influences complement system activation and whether previous kidney biopsy findings correspond with laboratory results.
- Conditions
- Diabetes, Diabetic Kidney Disease, Complement System
- Keywords
- diabetes, diabetic kidney disease, complement system, C3, CD59, MAC, MBL, C3a, C3b, C5a, new antidiabetic drugs
- Medical subject headings
- Diabetes Mellitus, Diabetic Nephropathies, Complement Component 3 Deficiency, Autosomal Recessive
What participants receive
What participants receive. In a randomised study each person is assigned to one group by chance.
| Study group | Role | What they receive |
|---|---|---|
| Patients with type 1 diabetes without chronic kidney disease | The investigators will include male and female patients aged between 40 and 65 years, who have diagnosis of diabetes for at least 10 years and no more than 25 years, with a body mass index below 30 kg/m², and without known macrovascular complications (coronary artery, peripheral arterial, or cerebrovascular disease). All participants must be treated with angiotensin-converting enzyme inhibitors or angiotensin receptor blockers at the highest tolerated dose. Individuals without known chronic kidney disease must meet kidney function criteria with an estimated glomerular filtration rate (eGFR) ≥ 60 ml/min and a urine albumin-to-creatinine ratio (UACR) < 3 g/mol. | |
| Patients with type 1 diabetes and chronic kidney disease | The investigators will include male and female patients aged between 40 and 65 years, who have diagnosis of diabetes for at least 10 years and no more than 25 years, with a body mass index below 30 kg/m², and without known macrovascular complications (coronary artery, peripheral arterial, or cerebrovascular disease). All participants must be treated with angiotensin-converting enzyme inhibitors or angiotensin receptor blockers at the highest tolerated dose. Individuals diagnosed with chronic kidney disease must meet the criteria of kidney function eGFR < 60 ml/min and UACR > 3 g/mol, or UACR > 30 g/mol regardless of eGFR. | |
| Patients with type 2 diabetes and chronic kidney disease | The investigators will include male and female patients aged between 40 and 65 years, who have diagnosis of diabetes for at least 10 years and no more than 25 years, with a body mass index below 30 kg/m², and without known macrovascular complications (coronary artery, peripheral arterial, or cerebrovascular disease). All participants must be treated with angiotensin-converting enzyme inhibitors or angiotensin receptor blockers at the highest tolerated dose. Individuals diagnosed with chronic kidney disease must meet the criteria of kidney function eGFR < 60 ml/min and UACR > 3 g/mol, or UACR > 30 g/mol regardless of eGFR. |
What is being measured
The primary outcome is the main question the study is designed to answer.
Level of complement system activation
The investigators will determine components of the complement system in blood and urine samples.
- Blood parameters:
- S compl. component C3: 0.6-1.3 g/L, ↓ consumpt.; ↑ inflam.,
- S compl. component C4: 0.1-0.3 g/L,↓ classical/lectin | ↑ inflam.,
- S fact. B: 166-399 mg/L, ↓ AP (alter. path.) consumpt. | ↑ AP act.,
- S fact. H: 380.6-674.9 mg/L, ↓ regul. | ↑ compensation,
- S fact. I: 21.2-42.1 mg/L, ↓ regul. | ↑ compensation,
- S soluble C5b-9 lytic complex (sC5b-9): 127-303 ng/mL, ↑ terminal compl.,
- S fact. B fragment Bb: 0.49-1.42 µg/mL, ↑ AP act.,
- S fact. H antibodies (anti-FH): < 10 U/mL, ↑ AP dysreg.,
- S C1q antibodies (anti-C1q): < 10 U/mL, ↑ classical pathway,
- S C3a: man.ref., ↑ compl. act.,
- S C3c: man. ref., ↑ C3 breakdown,
- S C5a: man. ref., ↑ strong act.
- Urine parameter :
- Urinary soluble C5b-9 lytic complex (sC5b-9): < 30 ng/mL, ↑ renal compl. act.
Expressed in different mass units (mg,g,µg,ng) or activity units (U) per volume units of blood serum (mL,L).
Measured: An additional visit to the diabetes outpatient clinic is planned within one year, where this will be determined.
Secondary outcomes (3)
IMT thickness
The investigators will measure the intima-media thickness (IMT) with ultrasound. Result will be expressed in millimetres. A thickness greater than 1.0 mm is considered pathological.
Measured: An additional visit to the diabetes outpatient clinic is planned within one year, where the examination will be performed.
Carotid-femoral pulse wave velocity (PWV)
The investigators will evaluate arterial stiffness and central hemodynamics non-invasively using applanation tonometry and pulse wave analysis. Results will be expressed in metres per second (m/s). Higher PWV values indicate increased arterial stiffness and reduced arterial elasticity. Augmentation Index (AIx), or AIx@75, represents the contribution of the reflected pulse wave to central systolic pressure and reflects arterial compliance and wave reflection. Higher AIx values indicate increased arterial stiffness and enhanced wave reflection. Because AIx is influenced by heart rate, it is commonly adjusted to a standardized heart rate of 75 beats per minute (AIx@75).
Measured: An additional visit to the diabetes outpatient clinic is planned within one year, where the examination will be performed.
Endothelial Function
The investigators will use peripheral arterial tonometry . The measurement is performed using a finger-mounted pneumatic probe, which detects pulsatile volume changes in the fingertip. The device's software analyses the change in pulse amplitude before and after occlusion, calculating the Reactive Hyperemia Index (RHI), which serves as a quantitative marker of endothelial function and has no unit. Lower RHI values indicate endothelial dysfunction and impaired nitric oxide-mediated vasodilation.Higher RHI values reflect preserved endothelial function.
Augmentation Index (AIx), derived from EndoPAT, reflects arterial stiffness and wave reflection in peripheral arteries. Higher AIx values indicate increased arterial stiffness and adverse vascular properties. Lower AIx values suggest better arterial compliance.
Measured: An additional visit to the diabetes outpatient clinic is planned within one year, where the examination will be performed.
Timeline
From the start of the study to its completion; the mark is today. Estimated dates are the sponsor’s plan.
- First posted18 Dec 2025
- Study start1 Dec 2025
- Primary completion31 Dec 2026 (estimated)
- Study completionDec 2028 (estimated)
Resources
- Official record on ClinicalTrials.govThe registry entry this page is built from, with its full change history.
- Publications (4)Papers the sponsor has linked to this study.
- Other trials for DiabetesStudies of the same condition, open and under way.
- More trials run by University Medical Centre LjubljanaThe 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
- Observational
- Observational model
- Cohort
- Time perspective
- Cross-sectional
- Enrolment
- 90 participants (estimated)
Sponsor and investigators
- Lead sponsor
- University Medical Centre Ljubljana
- Sponsor type
- University, hospital or other
- Responsible party
- Sponsor
- Investigators
- Miodrag Janić, Principal investigator
IDs, dates and publications
- ClinicalTrials.gov ID
- NCT07292493
- Sponsor's protocol ID
- 20250187
- Acronym
- KID-CODE
- Status last verified
- Nov 2025
- First submitted
- 19 Nov 2025
- Last updated
- 23 Feb 2026
- Results posted
- No
- Data monitoring committee
- No
- Individual data sharing
- Undecided
Publications
Li MR, Sun ZJ, Chang DY, Yu XJ, Wang SX, Chen M, Zhao MH. C3c deposition predicts worse renal outcomes in patients with biopsy-proven diabetic kidney disease in type 2 diabetes mellitus. J Diabetes. 2022 Apr;14(4):291-297. doi: 10.1111/1753-0407.13264. Epub 2022 Mar 24.
PubMed 35322566Ostergaard JA, Thiel S, Lajer M, Steffensen R, Parving HH, Flyvbjerg A, Rossing P, Tarnow L, Hansen TK. Increased all-cause mortality in patients with type 1 diabetes and high-expression mannan-binding lectin genotypes: a 12-year follow-up study. Diabetes Care. 2015 Oct;38(10):1898-903. doi: 10.2337/dc15-0851. Epub 2015 Jul 15.
PubMed 26180106Hansen TK, Tarnow L, Thiel S, Steffensen R, Stehouwer CD, Schalkwijk CG, Parving HH, Flyvbjerg A. Association between mannose-binding lectin and vascular complications in type 1 diabetes. Diabetes. 2004 Jun;53(6):1570-6. doi: 10.2337/diabetes.53.6.1570.
PubMed 15161763Flyvbjerg A. The role of the complement system in diabetic nephropathy. Nat Rev Nephrol. 2017 May;13(5):311-318. doi: 10.1038/nrneph.2017.31. Epub 2017 Mar 6.
PubMed 28262777
Study at a glance
From the registry record, last updated by the sponsor on 23 Feb 2026. Recruitment status is as the sponsor reported it: confirm with the study team.
- Official title
- The Role of Complement in Diabetic Kidney Disease
- ClinicalTrials.gov ID
- NCT07292493
- Acronym / sponsor ID
- KID-CODE / 20250187
- Conditions
- Diabetes, Diabetic Kidney Disease, Complement System
- Keywords
- diabetes, diabetic kidney disease, complement system, C3, CD59, MAC, MBL, C3a
- Study type
- Observational
- Recruitment status
- Enrolling by invitation
- Enrolment
- 90 participants (estimated)
- Lead sponsor
- University Medical Centre LjubljanaUniversity, hospital or other
- Study start
- 1 Dec 2025 (actual)
- Primary completion
- 31 Dec 2026 (estimated)
- Study completion
- Dec 2028 (estimated)
- First posted
- 18 Dec 2025 (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.
Diabetes is a chronic condition marked by long-term elevated blood glucose levels. There are more types of diabetes; the majority of patients have type 1 or type 2 diabetes. Over long period of time, high blood sugar damages blood vessels and organs. One of the most common complications is diabetic kidney disease, which can slowly lead to kidney failure. People with this condition also have a much higher risk of heart and blood vessel diseases.
Newer research shows that the immune system, especially the complement system (a group of proteins that help defend the body), may also play a role in worsening kidney disease in diabetes. High blood sugar can activate these proteins, and they have been found in kidney tissue of patients with diabetic kidney disease.
The goal of this study is to find out how much the complement system contributes to kidney damage in diabetes, whether it affects different groups of patients differently, and whether it is linked to blood vessel health or the stage of kidney disease. The study will also assess if improved diabetes control is linked to reduced complement system activity.
Detailed description
Diabetes is a chronic disease characterized by long-term elevated blood glucose levels. Several types of diabetes are known, with most affected individuals having type 1 or type 2 diabetes. Long-term elevation of blood glucose affects various organs in the body, a condition referred to as chronic complications of diabetes. Since elevated blood glucose damages both small and large blood vessels, complications are classified as microvascular (damage to small vessels) and macrovascular (damage to large vessels). Diabetic kidney disease is the main microvascular complication in both type 1 and type 2 diabetes and is also the leading cause of kidney failure.
Changes in the kidneys develop over many years. Gradual deterioration of kidney function is monitored using laboratory parameters. Along with declining kidney function, blood pressure also increases, and cardiovascular diseases begin to develop- the risk of these rises exponentially with worsening kidney function. Cardiovascular diseases represent the leading cause of mortality among people with diabetes.
Traditionally, diabetic kidney disease was considered as non-inflammatory condition. Its development was attributed to impaired glucose metabolism and elevated blood pressure. Consequently, achieving optimal blood glucose and blood pressure values has been regarded as key to preventing chronic complications. However, diabetes itself represents an additional risk factor for cardiovascular disease compared with individuals without diabetes. Thus, individuals with diabetic kidney disease are even more prone to cardiovascular events. In these patients it is especially important to follow treatment guidelines and to treat elevated blood glucose and blood pressure as intensively as possible. For individuals with diabetic kidney disease, medications from the group of angiotensin-converting enzyme inhibitors or angiotensin receptor blockers are prescribed for the treatment of high blood pressure. Both medication groups also have a protective effect on the kidneys and slow the decline of kidney function. Angiotensin is a substance in the body responsible for raising blood pressure-when its action is inhibited, blood pressure decreases.
The investigators now know that inflammation and the immune system also play a role in the development of chronic diabetic complications. The complement system (a group of proteins in the blood involved in immune responses) is becoming recognized for its importance. Current studies do not suggest that the complement system plays a key role in the onset of the disease; however, its role in the progression of diabetic kidney disease and possibly in the occurrence of different forms of the disease has become evident. Hyperglycaemia increases the activity of certain complement proteins and activates specific pathways, while the hyperglycaemic environment also impairs the regulation of some proteins. Kidney biopsies of individuals with diabetic kidney disease have shown the presence of complement proteins in kidney tissue, and gene expression analyses have identified activation of complement-related genes.
The purpose of this study is to determine whether and to what extent activation of the complement system contributes to diabetic kidney disease and to define potential differences among different groups of individuals with diabetes. Additionally, the investigators aim to determine whether there is a connection between complement system activation and arterial function, as well as between complement system activation and the stage of kidney disease. The investigators will also investigate whether diabetes control influences complement system activation and whether previous kidney biopsy findings correspond with laboratory results.
Study design
- Observational model
- Cohort
- Time perspective
- Cross-sectional
- Number of arms
- 3
| Arm | Type | Receives |
|---|---|---|
| Patients with type 1 diabetes without chronic kidney disease | – | –The investigators will include male and female patients aged between 40 and 65 years, who have diagnosis of diabetes for at least 10 years and no more than 25 years, with a body mass index below 30 kg/m², and without known macrovascular complications (coronary artery, peripheral arterial, or cerebrovascular disease). All participants must be treated with angiotensin-converting enzyme inhibitors or angiotensin receptor blockers at the highest tolerated dose. Individuals without known chronic kidney disease must meet kidney function criteria with an estimated glomerular filtration rate (eGFR) ≥ 60 ml/min and a urine albumin-to-creatinine ratio (UACR) < 3 g/mol. |
| Patients with type 1 diabetes and chronic kidney disease | – | –The investigators will include male and female patients aged between 40 and 65 years, who have diagnosis of diabetes for at least 10 years and no more than 25 years, with a body mass index below 30 kg/m², and without known macrovascular complications (coronary artery, peripheral arterial, or cerebrovascular disease). All participants must be treated with angiotensin-converting enzyme inhibitors or angiotensin receptor blockers at the highest tolerated dose. Individuals diagnosed with chronic kidney disease must meet the criteria of kidney function eGFR < 60 ml/min and UACR > 3 g/mol, or UACR > 30 g/mol regardless of eGFR. |
| Patients with type 2 diabetes and chronic kidney disease | – | –The investigators will include male and female patients aged between 40 and 65 years, who have diagnosis of diabetes for at least 10 years and no more than 25 years, with a body mass index below 30 kg/m², and without known macrovascular complications (coronary artery, peripheral arterial, or cerebrovascular disease). All participants must be treated with angiotensin-converting enzyme inhibitors or angiotensin receptor blockers at the highest tolerated dose. Individuals diagnosed with chronic kidney disease must meet the criteria of kidney function eGFR < 60 ml/min and UACR > 3 g/mol, or UACR > 30 g/mol regardless of eGFR. |
Who may qualify
- Ages
- 40 to 65 years
- Sex
- All
- Healthy volunteers
- Not accepted
- Age groups
- Adult, Older adult
- Study population
- Patients with type 1 and type 2 diabetes, who are being treated at the diabetology outpatient clinic of the Department of Endocrinology, Diabetes, and Metabolic Diseases, University Medical Centre Ljubljana.
Key inclusion criteria (3 listed)
- body mass index below 30 kg/m²
- unknown macrovascular complications
- treated with angiotensin-converting enzyme inhibitors or angiotensin receptor blockers at the highest tolerated dose
Key exclusion criteria (2 listed)
- a body mass index above 30 kg/m²
- macrovascular complications
Eligibility is decided by the study team after screening; this overview does not establish that a patient qualifies. Full inclusion and exclusion criteria.
Primary outcome
Level of complement system activation
Time frame: An additional visit to the diabetes outpatient clinic is planned within one year, where this will be determined.
The investigators will determine components of the complement system in blood and urine samples. * Blood parameters: * S compl. component C3: 0.6-1.3 g/L, ↓ consumpt.; ↑ inflam., * S compl. component C4: 0.1-0.3 g/L,↓ classical/lectin | ↑ inflam., * S fact. B: 166-399 mg/L, ↓ AP (alter. path.) consumpt. | ↑ AP act., * S fact. H: 380.6-674.9 mg/L, ↓ regul. | ↑ compensation, * S fact. I: 21.2-42.1 mg/L, ↓ regul. | ↑ compensation, * S soluble C5b-9 lytic complex (sC5b-9): 127-303 ng/mL, ↑ terminal compl., * S fact. B fragment Bb: 0.49-1.42 µg/mL, ↑ AP act., * S fact. H antibodies (anti-FH): < 10 U/mL, ↑ AP dysreg., * S C1q antibodies (anti-C1q): < 10 U/mL, ↑ classical pathway, * S C3a: man.ref., ↑ compl. act., * S C3c: man. ref., ↑ C3 breakdown, * S C5a: man. ref., ↑ strong act. * Urine parameter : * Urinary soluble C5b-9 lytic complex (sC5b-9): < 30 ng/mL, ↑ renal compl. act. Expressed in different mass units (mg,g,µg,ng) or activity units (U) per volume units of blood serum (mL,L).
3 secondary outcomes
IMT thickness
Time frame: An additional visit to the diabetes outpatient clinic is planned within one year, where the examination will be performed.
Carotid-femoral pulse wave velocity (PWV)
Time frame: An additional visit to the diabetes outpatient clinic is planned within one year, where the examination will be performed.
Endothelial Function
Time frame: An additional visit to the diabetes outpatient clinic is planned within one year, where the examination will be performed.
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 Feb 2026.
- Background: PubMed 35322566Li MR, Sun ZJ, Chang DY, Yu XJ, Wang SX, Chen M, Zhao MH. C3c deposition predicts worse renal outcomes in patients with biopsy-proven diabetic kidney disease in type 2 diabetes mellitus. J Diabetes. 2022 Apr;14(4):291-297. doi: 10.1111/1753-0407.13264. Epub 2022 Mar 24.
- Background: PubMed 26180106Ostergaard JA, Thiel S, Lajer M, Steffensen R, Parving HH, Flyvbjerg A, Rossing P, Tarnow L, Hansen TK. Increased all-cause mortality in patients with type 1 diabetes and high-expression mannan-binding lectin genotypes: a 12-year follow-up study. Diabetes Care. 2015 Oct;38(10):1898-903. doi: 10.2337/dc15-0851. Epub 2015 Jul 15.
- Background: PubMed 15161763Hansen TK, Tarnow L, Thiel S, Steffensen R, Stehouwer CD, Schalkwijk CG, Parving HH, Flyvbjerg A. Association between mannose-binding lectin and vascular complications in type 1 diabetes. Diabetes. 2004 Jun;53(6):1570-6. doi: 10.2337/diabetes.53.6.1570.
- Background: PubMed 28262777Flyvbjerg A. The role of the complement system in diabetic nephropathy. Nat Rev Nephrol. 2017 May;13(5):311-318. doi: 10.1038/nrneph.2017.31. Epub 2017 Mar 6.
- Individual participant dataSharing planned: Undecided
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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.
Miodrag Janić principal investigator
1 site in 1 country: see every site and its status.
Questions about this trial
What is this clinical trial studying?
An observational study of Diabetes and Diabetic Kidney Disease, run by University Medical Centre Ljubljana at 1 site in Slovenia.
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 3 inclusion and 2 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: enrolling by invitation, as of the sponsor's last update on 23 Feb 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 Slovenia. 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?
Level of complement system activation (time frame: An additional visit to the diabetes outpatient clinic is planned within one year, where this will be determined.). 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 NCT07292493, which also lists 4 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 Feb 2026.