Evidence map›Paper›PMID 32946006›Full record

ArticleClinical and experimental nephrology2021

Podocyte sphingomyelin phosphodiesterase acid-like 3b decreases among children with idiopathic nephrotic syndrome.

Shojiro Watanabe, Koji Hirono, Tomomi Aizawa, Koji Tsugawa, Kensuke Joh, Tadaatsu Imaizumi, Hiroshi Tanaka

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Article in Clinical and experimental nephrology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.

0numbers the graph read from it
0cells of the map it votes in
5citing papers in PubMed
0.4field-weighted citation impact, top 37% of its field
1 · What the graph read from it

What it found

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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

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3 · Its place in the literature

Who cites it

5 citing papers in PubMed, 11 citations in OpenAlex.

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4 · The record

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5 · Who and what money

Authors and funding

7 authors at 3 institutions in 1 country.

Shojiro WatanabeDepartment of Pediatrics, Hirosaki University Hospital, 51 Hon-cho, Hirosaki, 036-8563, Japan. swat4028@yahoo.co.jp.ORCID http://orcid.org/0000-0002-4379-5857
Koji HironoDepartment of Pediatrics, Hirosaki University Hospital, 51 Hon-cho, Hirosaki, 036-8563, Japan.
Tomomi AizawaDepartment of Pediatrics, Hirosaki University Hospital, 51 Hon-cho, Hirosaki, 036-8563, Japan.
Koji TsugawaDepartment of Pediatrics, Hirosaki University Hospital, 51 Hon-cho, Hirosaki, 036-8563, Japan.
Kensuke JohDepartment of Pathology, The Jikei University School of Medicine, Tokyo, Japan.
Tadaatsu ImaizumiDepartment of Vascular Biology, Hirosaki University Graduate School of Medicine, Hirosaki, Japan.
Hiroshi TanakaDepartment of Pediatrics, Hirosaki University Hospital, 51 Hon-cho, Hirosaki, 036-8563, Japan.
Hirosaki University Hospital · JPHirosaki University · JPJikei University School of Medicine · JP

Funding

JSPS KAKENHI JP16K19623
6 · The paper itself

Abstract

aimSphingomyelin phosphodiesterase acid-like 3b (SMPDL-3b), a regulator of the cytoskeleton, is expressed on podocytes. Recent reports present evidence that it is directly targeted by rituximab in the treatment of intractable nephrotic syndrome. However, the implications of SMPDL-3b for treatment of paediatric-onset idiopathic nephrotic syndrome (INS) remain unclear. This study aimed to investigate the level of expression of SMPDL-3b in urine, serum, and biopsy specimens and explore its implications in treatment of patients with INS.

methodsLevels of urinary SMPDL-3b among 31 patients (20 in remission and 11 in relapse) with INS were analysed by dot blotting. For reference of precise quantitative analysis, we examined urinary excretion of SMPDL-3b from 10 patients with INS by liquid chromatography-tandem mass spectrometry (LC-MS/MS) in both remitted and relapsed status. The levels of serum SMPDL-3b among 20 patients (13 in remission and 7 in relapse or onset) with INS were also measured using enzyme-linked immunosorbent assay. Further, the immunoreactivity of SMPDL-3b in the biopsy specimens obtained from patients with INS was compared with those from patients with proteinuric IgA nephropathy, lupus nephritis, and non-proteinuric controls.

resultsUrinary excretion of SMPDL-3b in patients with INS was significantly decreased in relapse cases compared with cases of remission and other types of proteinuric glomerular disease or controls by both dot blotting and LC-MS/MS method. On the other hand, serum SMPDL-3b level in INS was not different between cases of remission and relapse. Glomerular immunoreactivity of SMPDL-3b in patient with INS in remission was almost the same level to that of control.

conclusionThe expression of SMPDL-3b on podocytes is specifically decreased in paediatric-onset INS and its urinary excretion level reflects such conditions.

Indexed as

AdolescentCase-Control StudiesChildFemaleGlomerulonephritis, IGAHumansImmunologic FactorsLupus NephritisMaleNephrotic SyndromePodocytesProteinuriaRituximabSphingomyelin PhosphodiesteraseImmunologic FactorsRituximabSMPDL3B protein, humanSphingomyelin PhosphodiesteraseIdiopathic nephrotic syndromePodocytesRituximabSphingomyelin phosphodiesterase acid-like 3B

Identifiers

PMID32946006
OpenAlexW3087727299

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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.