ArticleKidney research and clinical practice2024
To treat or not to treat: CUBN-associated persistent proteinuria.
Article in Kidney research and clinical practice, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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Who cites it
4 citing papers in PubMed.
- Clinical course of proteinuria due to cubilin variants: a large multicenter pediatric cohort.Pediatric nephrology (Berlin, Germany) · 2026Article
- Clinical and Genetic Insights Into Isolated Proteinuria WithKidney international reports · 2026Article
- Structured Application of Genetic Testing in a Pediatric Kidney Clinic.Journal of the American Society of Nephrology : JASN · 2026Article
- Tubular proteinuria due to hereditary endocytic receptor disorder of the proximal tubule: Dent disease and chronic benign proteinuria.Pediatric nephrology (Berlin, Germany) · 2025Review
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6 authors.
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Abstract
backgroundPersistent proteinuria is an important indicator of kidney damage and requires active evaluation and intervention. However, tubular proteinuria of genetic origin typically does not improve with immunosuppression or antiproteinuric treatment. Recently, defects in CUBN were found to cause isolated proteinuria (mainly albuminuria) due to defective tubular albumin reuptake. Unlike most other genetically caused persistent albuminuria, CUBN C-terminal variants have a benign course without progression to chronic kidney disease according to the literature. Here, we present Korean cases with persistent proteinuria associated with C-terminal variants of CUBN.
methodsWe identified Korean patients with CUBN variants among those with an identified genetic cause of proteinuria and evaluated their clinical features and clinical course. We also reviewed the literature on CUBN-associated isolated proteinuria published to date and compared it with Korean patients.
resultsAll patients presented with incidentally found, asymptomatic isolated proteinuria at a median age of 5 years. The proteinuria was in the subnephrotic range and did not significantly change over time, regardless of renin- angiotensin system inhibition. Initial physical examination, laboratory findings, and kidney biopsy results, when available, were unremarkable other than significant proteinuria. All patients maintained kidney function throughout the follow-up duration. All patients had at least one splicing mutation, and most of the variants were located C-terminal side of the gene.
conclusionWe report Korean experience of CUBN-related benign proteinuria, that aligns with previous reports, indicating that this condition should be considered in cases with incidentally found asymptomatic isolated proteinuria, especially in young children.
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