Evidence map›Paper›PMID 41563417›Full record

ArticlePediatric nephrology (Berlin, Germany)2026

Corticosteroids augment cyclosporine nephrotoxicity in pediatric nephrotic syndrome: potential role of alternatively activated macrophages.

Tomomi Kondoh, Takuma Ando, Yuji Matsumoto, Masahiro Kaneko, Hiroya Hasegawa, Takeshi Yamada, Naonori Kumagai, David J Nikolic-Paterson, Yohei Ikezumi

Abstract read
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In one paragraph

Article in Pediatric nephrology (Berlin, Germany), 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

0numbers the graph read from it
0cells of the map it votes in
0citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

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

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

0 citing papers in PubMed.

No citing paper in PubMed yet.

4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

9 authors.

Tomomi KondohDepartment of Pediatrics, Fujita Health University School of Medicine, 1-98 Dengakugakubo, Kutsukake-Cho, Toyoake, Aichi, 470-1192, Japan.
Takuma AndoDepartment of Pediatrics, Fujita Health University School of Medicine, 1-98 Dengakugakubo, Kutsukake-Cho, Toyoake, Aichi, 470-1192, Japan.
Yuji MatsumotoDepartment of Pediatrics, Fujita Health University School of Medicine, 1-98 Dengakugakubo, Kutsukake-Cho, Toyoake, Aichi, 470-1192, Japan.
Masahiro KanekoDepartment of Pediatrics, Niigata University Medical and Dental Hospital, Niigata, Japan.
Hiroya HasegawaDepartment of Pediatrics, Niigata University Medical and Dental Hospital, Niigata, Japan.
Takeshi YamadaDepartment of Pediatrics, Niigata University Medical and Dental Hospital, Niigata, Japan.
Naonori KumagaiDepartment of Pediatrics, Fujita Health University School of Medicine, 1-98 Dengakugakubo, Kutsukake-Cho, Toyoake, Aichi, 470-1192, Japan.
David J Nikolic-PatersonDepartment of Nephrology and Monash University Department of Medicine, Monash Medical Centre, Clayton, VIC, Australia.
Yohei IkezumiDepartment of Pediatrics, Fujita Health University School of Medicine, 1-98 Dengakugakubo, Kutsukake-Cho, Toyoake, Aichi, 470-1192, Japan. ikezumi@fujita-hu.ac.jp.ORCID http://orcid.org/0000-0001-6460-1188

Funding

JSPS KAKENHI JP24K10988
6 · The paper itself

Abstract

backgroundCyclosporine A (CsA) is an effective steroid-sparing agent for steroid-dependent nephrotic syndrome (SDNS); however, long-term use can cause chronic kidney injury (CsA nephropathy). We previously reported that alternatively activated macrophages (M2-type) are linked to interstitial fibrosis in progressive kidney disease. This study aimed to investigate the potential involvement of M2-type macrophages in CsA nephropathy in SDNS.

methodsThirty-three children with SDNS treated with CsA for more than 2 years were investigated. Fourteen age-matched SDNS children without CsA served as controls. Kidney fibrosis was assessed by Masson staining. Sections were immunostained for α-SMA, type I collagen, CD68, CD163, and CCL2. Urine levels of CCL2 were measured using a cytometric bead array kit.

resultsThe CsA-treated group showed greater interstitial fibrosis (12.2 ± 7.3 vs.7.6 ± 2.1%, p < 0.001) and increased CD163

conclusionCD163

Indexed as

Adrenal Cortex HormonesCyclosporineImmunosuppressive AgentsKidneyMacrophage ActivationMacrophagesNephrotic SyndromePrednisoloneAdolescentAntigens, CDAntigens, Differentiation, MyelomonocyticBiopsyCD163 AntigenCD68 MoleculeChemokine CCL2ChildAdrenal Cortex HormonesAntigens, CDAntigens, Differentiation, MyelomonocyticCCL2 protein, humanCD163 AntigenCD68 antigen, humanCD68 MoleculeChemokine CCL2CyclosporineImmunosuppressive AgentsPrednisoloneReceptors, Cell SurfaceCCL2CyclosporineFibrosis, Nephrotic syndromeM2-type macrophage

Identifiers

PMID41563417

What Socratic holds

Textmetadata
Read underepoch 390

Registered trials

None linked

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 Socratic graph.