ArticlePediatric nephrology (Berlin, Germany)2026
Unveiling long-standing low-molecular-weight proteinuria: A proximal tubular mitochondrial enzyme impairment caused by EHHADH mutation.
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. Cited by 2 papers.
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2 citing papers in PubMed.
- Network Pharmacology Combined With Metabonomics and Transcriptomics Reveals the Mechanism ofFood science & nutrition · 2026Article
- Genetic Screening of Patients With Inherited Fanconi Syndrome.Kidney international reports · 2026Article
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6 authors.
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Abstract
The energy requirement of renal proximal tubular cells depends on mitochondrial fatty acid β-oxidation. Enoyl-CoA hydratase-l-3-hydroxyacyl-CoA dehydrogenase (EHHADH) is a crucial enzyme in mitochondrial fatty acid oxidation, and mutations in EHHADH reportedly cause Fanconi syndrome. Here, we report the case of a 28-year-old Japanese woman with a long-term history of low-molecular-weight proteinuria (LMWP) who exhibited a missense mutation in the EHHADH gene. She was diagnosed with LMWP at 4 years of age. The search for the CLCN5 gene was unremarkable, and kidney biopsy revealed no significant tubulointerstitial changes. The LMWP persisted, and glucosuria gradually developed thereafter. Unexpectedly, next-generation sequencing identified a heterozygous missense mutation in the EHHADH gene. Her father, who harbored LMWP, also had the same mutation. Furthermore, immunostaining of the stored kidney specimens showed decreased immunoreactivity for cytochrome c oxidase subunit 4 in the proximal tubules, suggesting an underlying mitochondrial impairment.
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