2017 Fiscal Year Final Research Report
The B cell independent mechanism of Rituximab in Pediatric-Onset Intractable Nephrotic Syndrome.
| Project/Area Number |
16K19623
|
|---|
| Research Category |
Grant-in-Aid for Young Scientists (B)
|
| Allocation Type | Multi-year Fund |
|---|
| Research Field |
Pediatrics
|
|---|
| Research Institution | Hirosaki University |
|---|
Principal Investigator |
|
|---|
| Project Period (FY) |
2016-04-01 – 2018-03-31
|
| Keywords | ネフローゼ症候群 / SMPDL3b / リツキシマブ |
|---|
| Outline of Final Research Achievements |
To examine the role of SMPDL3b in the pathogenesis of NS, we examined urinary excretion of SMPDL3b by using dot blotting. Urinary excretion of SMPDL3b in patients with heavy proteinuric NS was significantly decreased compared to that in patients in remission, those with IgA nephropathy/vasculitis, and controls.
These findings suggest that changes in SMPDL3b expression on the podocyte probably occur in pediatric-onset NS. Among them, RTX may work on podocyte in SMPDL3b-dependent manner, suggesting that low expressions of SMPDL3b in urine and glomerular immunoreactivity even in remission resulted in the RTX-resistance. Although detailed mechanism of downregulation of SMPDL3b expression remains to be elucidated, SMPDL3b is, at least in part, involved in the pathogenesis of pediatric-onset NS. In addition, measurement of urinary excretion of SMPDL3b could be a possible in invasive biomarker to predict reactivity to rituximab therapy in pediatric onset nephrotic syndrome.
|
| Free Research Field |
小児腎臓病学
|
