# Pediatric-Onset Multiple Sclerosis at Age 10 Following Nephrotic Syndrome: Early Recognition and Successful Treatment With Fingolimod

**Authors:** Imane Mezdaoui, Khadija Mouaddine, Chaimae Nahi, Bouchra Chkirate

PMC · DOI: 10.7759/cureus.103071 · Cureus · 2026-02-05

## TL;DR

A 10-year-old boy with rare pediatric-onset multiple sclerosis was successfully treated with fingolimod after advanced MRI and CSF analysis confirmed the diagnosis.

## Contribution

Demonstrates successful treatment of very early-onset multiple sclerosis using fingolimod and highlights the role of advanced MRI biomarkers in diagnosis.

## Key findings

- Advanced MRI biomarkers, including central vein sign and paramagnetic rim, supported the MS diagnosis in a 10-year-old.
- Fingolimod treatment led to complete clinical and radiological suppression of MS over 18 months.
- Early initiation of high-efficacy therapy improved outcomes in a rare pediatric MS case.

## Abstract

Pediatric-onset multiple sclerosis before the age of 10 is rare and poses significant diagnostic challenges. We report a 10-year-old boy who developed multiple sclerosis five years after remission of nephrotic syndrome. He presented with progressive left eye visual loss and vertigo. Advanced magnetic resonance imaging (MRI) revealed demyelinating lesions with a central vein sign and paramagnetic rim, emerging biomarkers that support the diagnosis of pediatric multiple sclerosis. Cerebrospinal fluid analysis demonstrated type 2 oligoclonal bands, while anti-aquaporin-4 and anti-myelin oligodendrocyte glycoprotein antibodies were negative. The diagnosis of multiple sclerosis was established according to the 2017 McDonald criteria. Early treatment with fingolimod (0.5 mg daily) resulted in complete clinical and radiological disease suppression over an 18-month follow-up period. This case highlights the value of advanced MRI biomarkers in very early-onset multiple sclerosis, the importance of systematically excluding disease mimics in prepubertal children, and the effectiveness of early initiation of high-efficacy disease-modifying therapy. Early recognition and prompt treatment are essential to optimize outcomes in pediatric multiple sclerosis.

## Linked entities

- **Proteins:** AQP4 (aquaporin 4)
- **Chemicals:** fingolimod (PubChem CID 107970)
- **Diseases:** multiple sclerosis (MONDO:0005301), nephrotic syndrome (MONDO:0005377)

## Full-text entities

- **Genes:** AQP4 (aquaporin 4) [NCBI Gene 361] {aka MIWC, MLC4, WCH4, hAQP4}, HLA-A (major histocompatibility complex, class I, A) [NCBI Gene 3105] {aka HLAA}, MOG (myelin oligodendrocyte glycoprotein) [NCBI Gene 4340] {aka BTN6, BTNL11, MOGIG2, NRCLP7}
- **Diseases:** lymphocytic pleocytosis (MESH:D007964), macular edema (MESH:D008269), infection (MESH:D007239), optic neuritis (MESH:D009902), infectious or post-infectious demyelination (MESH:D000094025), Periventricular lesions (MESH:D054091), MOG antibody-associated disease (MESH:D003711), encephalopathy (MESH:D001927), MS (MESH:D009103), immune dysregulation (OMIM:614878), NMOSD (MESH:D009471), lymphopenia (MESH:D008231), left eye vision loss (MESH:D014786), optic atrophy (MESH:D009896), Nephrotic Syndrome (MESH:D009404), relative afferent pupillary defect (MESH:D011681), inflammation (MESH:D007249), optic nerve dysfunction (MESH:D000080344), ADEM (MESH:D004673), metabolic (MESH:D008659), vertigo (MESH:D014717), hyperemia (MESH:D006940), strabismus (MESH:D013285), genetic leukodystrophies (MESH:D007966), periventricular white matter lesion (MESH:D056784), autoimmune diseases (MESH:D001327)
- **Chemicals:** Fingolimod (MESH:D000068876)
- **Species:** Homo sapiens (human, species) [taxon 9606]

## Full text

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## Figures

2 figures with captions in the complete paper: https://tomesphere.com/paper/PMC12968079/full.md

## References

16 references — full list in the complete paper: https://tomesphere.com/paper/PMC12968079/full.md

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Source: https://tomesphere.com/paper/PMC12968079