Evidence map›Paper›PMID 39913008›Full record

ArticleCEN case reports2025

Case of maternal uniparental isodisomy with autosomal recessive Alport syndrome combined with congenital myasthenia and Oguchi disease.

Misaki Akiyama, Keiko Matsubara, Hiroshi Terashima, Yuichi Abe, Kinji Ohno, Koichi Kamei

Abstract readCase Reports
In one paragraph

Article in CEN case reports, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

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4 · The record

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5 · Who and what money

Authors and funding

6 authors.

Misaki AkiyamaDivision of Nephrology and Rheumatology, National Center for Child Health and Development, 2-10-1 Okura, Setagaya-Ku, Tokyo, 157-8535, Japan.
Keiko MatsubaraDivision of Diversity Research, National Center for Child Health and Development, Tokyo, Japan.
Hiroshi TerashimaDepartment of Pediatrics, The University of Tokyo Hospital, Tokyo, Japan.
Yuichi AbeDivision of Neurology, National Center for Child Health and Development, Tokyo, Japan.
Kinji OhnoDivision of Neurogenetics, Center for Neurological Diseases and Cancer, Nagoya University Graduate School of Medicine, Aichi, Japan.
Koichi KameiDivision of Nephrology and Rheumatology, National Center for Child Health and Development, 2-10-1 Okura, Setagaya-Ku, Tokyo, 157-8535, Japan. kamei-k@ncchd.go.jp.ORCID 0000-0003-3528-6961

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Uniparental isodisomy (UPiD) is a genetic condition in which an individual inherits two identical copies of a chromosome, or part of a chromosome, from one parent. UPiD can result in the development of autosomal recessive disorders if the chromosome inherited from one parent has a pathogenic variant. Herein, we present a 20 year-old female patient who had no significant family history including kidney, muscular, or ocular diseases. She had muscle weakness since infancy and was suspected with congenital myasthenia. She was diagnosed with Oguchi disease, a congenital condition characterized by night blindness, by an ophthalmologist. At 3 years of age, hematuria was noted, and gross hematuria was occasionally observed thereafter. Exome analysis revealed homozygous variants in the COL4A4, CHRND, and SAG genes on chromosome 2, which are the causative genes of Alport syndrome, congenital myasthenic syndrome, and Oguchi disease, respectively. Array comparative genomic hybridization analysis and microsatellite analysis revealed maternal UPiD. At approximately 18 years of age, she presented with proteinuria with mild kidney impairment, and kidney biopsy was performed at 20 years of age. Type IV collagen α5 chain staining showed a weak but positive image in the glomerular basement membrane. However, thinning and irregular thickening of the glomerular basement membrane and reticular changes in the dense layer were observed, which were consistent with Alport syndrome. Angiotensin II receptor blocker (candesartan) was administered, and her urinary protein levels decreased. She had a homozygous missense variant, positive α5 chain staining, and a mild phenotype.

Indexed as

Myasthenic Syndromes, CongenitalNephritis, HereditaryUniparental DisomyCollagen Type IVFemaleHematuriaHumansYoung AdultCOL4A4 protein, humanCollagen Type IVAlport syndromeAutosomal recessive heredityCongenital myastheniaOguchi diseaseUniparental isodisomy

Identifiers

PMID39913008
PMCPMC12126394

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