T-regulatory Cells in Diabetic Type Two Nephropathy

Status Not yet recruiting

Clinical Trial Summary

Diabetes mellitus is one of the most prevalent health problems worldwide. Diabetic nephropathy has become the leading cause of end-stage kidney disease worldwide and is associated with an increased cardiovascular risk.

Traditionally, metabolic and hemodynamic factors are the main causes of renal lesions in patients with type two diabetes mellitus and diabetic nephropathy , both considered non-immune diseases. Serial researches has demonstrated that diabetic nephropathy is a metabolic and hemodynamic disorder, with inflammation playing a vital role in the process.

Clinical Trial Description

It has been reported that glomerular basement membranes from diabetic rats induced significantly greater amounts of Tumor necrotic factor-alpha and Interleukin-1 than when these cells were incubated with basement membranes from non-diabetic rats.

These new findings were the first to suggest that inflammatory cytokines may participate in the pathogenesis of diabetic nephropathy .Cluster of differentiation 4 cells are believed to play central roles in modulating immune responses. Tumor necrotic factor-alpha and Interleukin-6, and induce inflammation in the pathogenesis of autoimmune diseases.

T- regulatory cells exert immunosuppressive effects which are important on the maintenance of immune homeostasis by producing anti-inflammatory cytokines, such as Interleukin-10 and transforming growth factor-b.

Aim of this work is to the role of T regulatory cells :( Cluster of differentiation 4, Cluster of differentiation 25,Cluster of differentiation 127 , forkhead box P3 cells) in the different stages of diabetic nephropathy before hemodialysis initiation. ;

Study Design

Related Conditions & MeSH terms

Clinical Trial Details

NCT number	NCT03591939
Study type	Observational
Source	Assiut University
Contact	Muhammed Hossam Maghraby, professor
Phone	00201020671222
Email	hossammaghraby@med.au.edu.eg
Status	Not yet recruiting
Phase
Start date	August 1, 2018
Completion date	October 1, 2019

View Details

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