Glomerular DiseaseNCT05875454
Podocyts Integrity in Glomerular Diseases
An observational study of Glomerular Disease, run by Assiut University.
Trial summary
To assess the density and ultrastructural morphology of podocytes in different glomerular diseases. Correlate the podocyte density and ultrastuctural morphology with laboratory data, the histopathological diagnosis and the active and chronic histopathological lesions in the biopsy. Read more about this study
- Who is it for?
- Ages 10 to 75 years
- Conditions the study is for
- Glomerular Disease
- What is being tested?
- Histopathological examination of tru-cut needle biopsy
- How many people
- 50 participants
- Where
- No sites listed yet
- Study dates
- Jul 2023to Dec 2025
- Phase
- Observational
- Are there results?
- None posted in the registry
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 10 to 75 years
- All sexes
- Child, Adult, Older adult
Study population: Patients suspected to have medical renal disease.
Who may be able to join
- Patients undergoing renal biopsy and diagnosed as glomerular disease.
Who cannot join
- Patients diagnosed as tubule-interstitial diseases.
Trial locations and contacts
No sites are listed yet.
About this study
Official title: Assessment of Podocyts Integrity in Glomerular Diseases.
- To assess the density and ultrastructural morphology of podocytes in different glomerular diseases.
- Correlate the podocyte density and ultrastuctural morphology with laboratory data, the histopathological diagnosis and the active and chronic histopathological lesions in the biopsy.
Read the detailed description
Glomerular diseases are common causes of end-stage renal failure. Increasing evidence suggests that these glomerulopathies are frequently caused by primary lesions in the renal podocytes. Podocytes are highly specialized glomerular epithelial cells that form the glomerular filtration barrier together with the fenestrated endothelium and the glomerular basement membrane. The podocyte cell body bulges into the urinary space and gives long processes that branch into foot processes, enwrapping the glomerular capillaries. Adjacent podocytes interdigitate with each other at their foot processes which are bridged with a specialized intercellular junction called a slit diaphragm, which is evenly spaced areas covered by slit diaphragm proteins that facilitate podocyte-to-podocyte contact.
Podocytes live under various stresses and pathological stimuli. They adapt to maintain homeostasis, but excessive stress leads to maladaptation and injury. Podocyte injury causes proteinuria, ranging from albuminuria to massive nephrotic syndrome. The integrity of podocytes and their interaction with the glomerular basement membrane is crucial for maintenance of the intact glomerular filtration barrier. Alteration of the intercellular junctions and cytoskeletal structure of podocytes or their detachment from the membrane results in the development of albuminuria. Podocyte density is one of the best predictors of the progression in glomerular diseases. The number of podocytes seems to be very critical for kidney health as the loss of podocytes results in glomerular damage. Thus, the extent of podocyte damage and loss seems to define the progression rate in many kidney disease.
As podocytes have limited ability to repair and/or regenerate, the extent of podocyte injury is a major prognostic determinant in glomerular diseases. Therapies aimed at preventing or limiting podocyte injury and/or at promoting podocyte repair or regeneration therefore have major potential benefits. Podocytes display a remarkable ability to recover from complete effacement and to re-form interdigitating foot processes and intact slit diaphragms after pharmacological intervention.
Podocytes are the main sites of expression of the wilm's tumor suppressor gene, WT1, in the adult. WT1 is a complex gene, which plays an essential role in renal development by controlling the process of mesenchymal to epithelial transition that form the nephron. Adult podocyte maintains both epithelial and mesenchymal features and continue to express high levels of WT1. Several lines of evidence suggest that WT1 may indeed play an important role in the maintenance of normal podocyte function. Mutations in Wilms' tumor 1 cause a wide spectrum of renal manifestations, eventually leading to end-stage kidney failure. WT1 mutations have been found to cause up to 12 % of steroid resistant nephrotic syndrome in children and young adults, particularly in phenotypic females.
- Conditions
- Glomerular Disease
- Being tested
- Histopathological examination of tru-cut needle biopsy
What participants receive
What participants receive. In a randomised study each person is assigned to one group by chance.
Histopathological examination of tru-cut needle biopsyDiagnostic test
Renal biopsies fixed in formalin from patients with suspected medical renal disease will be processed and examined for histopathological diagnosis.
What is being measured
The primary outcome is the main question the study is designed to answer.
assessment of podocytes integrity in different glomerular disaeses.
Assessment of podocytes density which will be detected by immunohistochemical expression of WT-1 in different glomerular diseases.
Correletion between the podocytes density with laboratory data of the cases and the histopathological diagnosis.
Measured: 14 months
Timeline
From the start of the study to its completion; the mark is today. Estimated dates are the sponsor’s plan.
- First posted25 May 2023
- Study startJul 2023 (estimated)
- Primary completionNov 2025 (estimated)
- Study completionDec 2025 (estimated)
Resources
- Official record on ClinicalTrials.govThe registry entry this page is built from, with its full change history.
- Publications (10)Papers the sponsor has linked to this study.
- Other trials for Glomerular DiseaseStudies of the same condition, open and under way.
- More trials run by Assiut UniversityThe 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
- Case only
- Time perspective
- Prospective
- Enrolment
- 50 participants (estimated)
Sponsor and investigators
- Lead sponsor
- Assiut University
- Sponsor type
- University, hospital or other
- Responsible party
- Principal investigator, Aya Salah Rashed, Assiut University
IDs, dates and publications
- ClinicalTrials.gov ID
- NCT05875454
- Sponsor's protocol ID
- podocytes in glomeruli
- Status last verified
- Jun 2023
- First submitted
- 30 Apr 2023
- Last updated
- 12 Jun 2023
- Results posted
- No
- Data monitoring committee
- No
- FDA-regulated drug
- No
- FDA-regulated device
- No
Publications
Guo JK, Menke AL, Gubler MC, Clarke AR, Harrison D, Hammes A, Hastie ND, Schedl A. WT1 is a key regulator of podocyte function: reduced expression levels cause crescentic glomerulonephritis and mesangial sclerosis. Hum Mol Genet. 2002 Mar 15;11(6):651-9. doi: 10.1093/hmg/11.6.651.
PubMed 11912180Barutta F, Bellini S, Gruden G. Mechanisms of podocyte injury and implications for diabetic nephropathy. Clin Sci (Lond). 2022 Apr 14;136(7):493-520. doi: 10.1042/CS20210625.
PubMed 35415751Sever S. Role of actin cytoskeleton in podocytes. Pediatr Nephrol. 2021 Sep;36(9):2607-2614. doi: 10.1007/s00467-020-04812-z. Epub 2020 Nov 13.
PubMed 33188449Kravets I, Mallipattu SK. The Role of Podocytes and Podocyte-Associated Biomarkers in Diagnosis and Treatment of Diabetic Kidney Disease. J Endocr Soc. 2020 Mar 5;4(4):bvaa029. doi: 10.1210/jendso/bvaa029. eCollection 2020 Apr 1.
PubMed 32232184Nagata M. Podocyte injury and its consequences. Kidney Int. 2016 Jun;89(6):1221-30. doi: 10.1016/j.kint.2016.01.012. Epub 2016 Mar 19.
PubMed 27165817Dong L, Pietsch S, Englert C. Towards an understanding of kidney diseases associated with WT1 mutations. Kidney Int. 2015 Oct;88(4):684-90. doi: 10.1038/ki.2015.198. Epub 2015 Jul 8.
PubMed 26154924Lal MA, Patrakka J. Understanding Podocyte Biology to Develop Novel Kidney Therapeutics. Front Endocrinol (Lausanne). 2018 Jul 23;9:409. doi: 10.3389/fendo.2018.00409. eCollection 2018.
PubMed 30083135Mathieson PW. The podocyte as a target for therapies--new and old. Nat Rev Nephrol. 2011 Nov 1;8(1):52-6. doi: 10.1038/nrneph.2011.171.
PubMed 22045242Muller-Deile J, Schiffer M. Podocyte directed therapy of nephrotic syndrome-can we bring the inside out? Pediatr Nephrol. 2016 Mar;31(3):393-405. doi: 10.1007/s00467-015-3116-4. Epub 2015 May 5.
PubMed 25939817Testagrossa L, Azevedo Neto R, Resende A, Woronik V, Malheiros D. Immunohistochemical expression of podocyte markers in the variants of focal segmental glomerulosclerosis. Nephrol Dial Transplant. 2013 Jan;28(1):91-8. doi: 10.1093/ndt/gfs325. Epub 2012 Aug 1.
PubMed 22859792
Study at a glance
From the registry record, last updated by the sponsor on 12 Jun 2023. Recruitment status is as the sponsor reported it: confirm with the study team.
- Official title
- Assessment of Podocyts Integrity in Glomerular Diseases.
- ClinicalTrials.gov ID
- NCT05875454
- Acronym / sponsor ID
- podocytes in glomeruli
- Conditions
- Glomerular Disease
- Study type
- Observational
- Recruitment status
- Unknown status
- Enrolment
- 50 participants (estimated)
- Lead sponsor
- Assiut UniversityUniversity, hospital or other
- Study start
- Jul 2023 (estimated)
- Primary completion
- Nov 2025 (estimated)
- Study completion
- Dec 2025 (estimated)
- First posted
- 25 May 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.
- To assess the density and ultrastructural morphology of podocytes in different glomerular diseases.
- Correlate the podocyte density and ultrastuctural morphology with laboratory data, the histopathological diagnosis and the active and chronic histopathological lesions in the biopsy.
Detailed description
Glomerular diseases are common causes of end-stage renal failure. Increasing evidence suggests that these glomerulopathies are frequently caused by primary lesions in the renal podocytes. Podocytes are highly specialized glomerular epithelial cells that form the glomerular filtration barrier together with the fenestrated endothelium and the glomerular basement membrane. The podocyte cell body bulges into the urinary space and gives long processes that branch into foot processes, enwrapping the glomerular capillaries. Adjacent podocytes interdigitate with each other at their foot processes which are bridged with a specialized intercellular junction called a slit diaphragm, which is evenly spaced areas covered by slit diaphragm proteins that facilitate podocyte-to-podocyte contact.
Podocytes live under various stresses and pathological stimuli. They adapt to maintain homeostasis, but excessive stress leads to maladaptation and injury. Podocyte injury causes proteinuria, ranging from albuminuria to massive nephrotic syndrome. The integrity of podocytes and their interaction with the glomerular basement membrane is crucial for maintenance of the intact glomerular filtration barrier. Alteration of the intercellular junctions and cytoskeletal structure of podocytes or their detachment from the membrane results in the development of albuminuria. Podocyte density is one of the best predictors of the progression in glomerular diseases. The number of podocytes seems to be very critical for kidney health as the loss of podocytes results in glomerular damage. Thus, the extent of podocyte damage and loss seems to define the progression rate in many kidney disease.
As podocytes have limited ability to repair and/or regenerate, the extent of podocyte injury is a major prognostic determinant in glomerular diseases. Therapies aimed at preventing or limiting podocyte injury and/or at promoting podocyte repair or regeneration therefore have major potential benefits. Podocytes display a remarkable ability to recover from complete effacement and to re-form interdigitating foot processes and intact slit diaphragms after pharmacological intervention.
Podocytes are the main sites of expression of the wilm's tumor suppressor gene, WT1, in the adult. WT1 is a complex gene, which plays an essential role in renal development by controlling the process of mesenchymal to epithelial transition that form the nephron. Adult podocyte maintains both epithelial and mesenchymal features and continue to express high levels of WT1. Several lines of evidence suggest that WT1 may indeed play an important role in the maintenance of normal podocyte function. Mutations in Wilms' tumor 1 cause a wide spectrum of renal manifestations, eventually leading to end-stage kidney failure. WT1 mutations have been found to cause up to 12 % of steroid resistant nephrotic syndrome in children and young adults, particularly in phenotypic females.
Study design
- Observational model
- Case only
- Time perspective
- Prospective
Who may qualify
- Ages
- 10 to 75 years
- Sex
- All
- Age groups
- Child, Adult, Older adult
- Study population
- Patients suspected to have medical renal disease.
Key inclusion criteria (1 listed)
- Patients undergoing renal biopsy and diagnosed as glomerular disease.
Key exclusion criteria (1 listed)
- Patients diagnosed as tubule-interstitial diseases.
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 |
|---|---|---|
| Histopathological examination of tru-cut needle biopsyRenal biopsies fixed in formalin from patients with suspected medical renal disease will be processed and examined for histopathological diagnosis. | Diagnostic test | – |
Primary outcome
assessment of podocytes integrity in different glomerular disaeses.
Time frame: 14 months
Assessment of podocytes density which will be detected by immunohistochemical expression of WT-1 in different glomerular diseases. Correletion between the podocytes density with laboratory data of the cases and the histopathological diagnosis.
Results and safety
Results are not available in the source record.
Research links
- Official record on ClinicalTrials.govLast updated by the sponsor 12 Jun 2023.
- Background: PubMed 11912180Guo JK, Menke AL, Gubler MC, Clarke AR, Harrison D, Hammes A, Hastie ND, Schedl A. WT1 is a key regulator of podocyte function: reduced expression levels cause crescentic glomerulonephritis and mesangial sclerosis. Hum Mol Genet. 2002 Mar 15;11(6):651-9. doi: 10.1093/hmg/11.6.651.
- Background: PubMed 35415751Barutta F, Bellini S, Gruden G. Mechanisms of podocyte injury and implications for diabetic nephropathy. Clin Sci (Lond). 2022 Apr 14;136(7):493-520. doi: 10.1042/CS20210625.
- Background: PubMed 33188449Sever S. Role of actin cytoskeleton in podocytes. Pediatr Nephrol. 2021 Sep;36(9):2607-2614. doi: 10.1007/s00467-020-04812-z. Epub 2020 Nov 13.
- Background: PubMed 32232184Kravets I, Mallipattu SK. The Role of Podocytes and Podocyte-Associated Biomarkers in Diagnosis and Treatment of Diabetic Kidney Disease. J Endocr Soc. 2020 Mar 5;4(4):bvaa029. doi: 10.1210/jendso/bvaa029. eCollection 2020 Apr 1.
- Background: PubMed 27165817Nagata M. Podocyte injury and its consequences. Kidney Int. 2016 Jun;89(6):1221-30. doi: 10.1016/j.kint.2016.01.012. Epub 2016 Mar 19.
- Background: PubMed 26154924Dong L, Pietsch S, Englert C. Towards an understanding of kidney diseases associated with WT1 mutations. Kidney Int. 2015 Oct;88(4):684-90. doi: 10.1038/ki.2015.198. Epub 2015 Jul 8.
- Background: PubMed 30083135Lal MA, Patrakka J. Understanding Podocyte Biology to Develop Novel Kidney Therapeutics. Front Endocrinol (Lausanne). 2018 Jul 23;9:409. doi: 10.3389/fendo.2018.00409. eCollection 2018.
- Background: PubMed 22045242Mathieson PW. The podocyte as a target for therapies--new and old. Nat Rev Nephrol. 2011 Nov 1;8(1):52-6. doi: 10.1038/nrneph.2011.171.
- Background: PubMed 25939817Muller-Deile J, Schiffer M. Podocyte directed therapy of nephrotic syndrome-can we bring the inside out? Pediatr Nephrol. 2016 Mar;31(3):393-405. doi: 10.1007/s00467-015-3116-4. Epub 2015 May 5.
- Background: PubMed 22859792Testagrossa L, Azevedo Neto R, Resende A, Woronik V, Malheiros D. Immunohistochemical expression of podocyte markers in the variants of focal segmental glomerulosclerosis. Nephrol Dial Transplant. 2013 Jan;28(1):91-8. doi: 10.1093/ndt/gfs325. Epub 2012 Aug 1.
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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.
Questions about this trial
What is this clinical trial studying?
An observational study of Glomerular Disease, run by Assiut University.
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 1 inclusion and 1 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: status not confirmed, as of the sponsor's last update on 12 Jun 2023. Status can change between updates, so confirm with the study contact before making plans.
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?
Results are not available in the source record.
How can a doctor refer a patient or contact the research team?
Contact Aya Salah, administrator (01095538980, ayaasalah23@gmail.com), or a site near the patient. AzTrials does not enrol participants or take referrals.
What does the primary outcome measure?
assessment of podocytes integrity in different glomerular disaeses. (time frame: 14 months). 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 NCT05875454, which also lists 10 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 12 Jun 2023.