Viewing Study NCT05875454



Ignite Creation Date: 2024-05-06 @ 7:03 PM
Last Modification Date: 2024-10-26 @ 2:59 PM
Study NCT ID: NCT05875454
Status: NOT_YET_RECRUITING
Last Update Posted: 2023-06-12
First Post: 2023-04-30

Brief Title: Podocyts Integrity in Glomerular Diseases
Sponsor: Assiut University
Organization: Assiut University

Study Overview

Official Title: Assessment of Podocyts Integrity in Glomerular Diseases
Status: NOT_YET_RECRUITING
Status Verified Date: 2023-06
Last Known Status: None
Delayed Posting: No
If Stopped, Why?: Not Stopped
Has Expanded Access: False
If Expanded Access, NCT#: N/A
Has Expanded Access, NCT# Status: N/A
Acronym: None
Brief 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
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 andor regenerate the extent of podocyte injury is a major prognostic determinant in glomerular diseases Therapies aimed at preventing or limiting podocyte injury andor 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 wilms 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 Oversight

Has Oversight DMC: None
Is a FDA Regulated Drug?: False
Is a FDA Regulated Device?: False
Is an Unapproved Device?: None
Is a PPSD?: None
Is a US Export?: None
Is an FDA AA801 Violation?: None