ArticleInternational journal of molecular sciences2022
Hematopoietic Disorders, Renal Impairment and Growth in Mucopolysaccharidosis-Plus Syndrome.
Article in International journal of molecular sciences, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
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Who cites it
12 citing papers in PubMed, 15 citations in OpenAlex.
- Severe neurodevelopmental phenotype with multisystem involvement in VPS16-related mucopolysaccharidosis-like syndrome.Neurogenetics · 2026Article
- Cellular and molecular changes in mucopolysaccharidosis-plus syndrome caused by a homozygous c.599G > C (p.Arg200Pro) variant of the VPS33A gene.Journal of applied genetics · 2026Article
- Explainable AI-driven graph-based neural networks for mucopolysaccharidoses diagnosis.BioData mining · 2026Article
- The use of genistein and ambroxol may be an effective approach in correcting cellular dysfunctions of mucopolysaccharidosis-plus syndrome.Mammalian genome : official journal of the International Mammalian Genome Society · 2025Article
- Mucopolysaccharidoses-What Clinicians Need to Know: A Clinical, Biochemical, and Molecular Overview.Biomolecules · 2025Review
- Article
- Screening core genes for minimal change disease based on bioinformatics and machine learning approaches.International urology and nephrology · 2025Article
- Mucopolysaccharidosis-Plus Syndrome: Is This a Type of Mucopolysaccharidosis or a Separate Kind of Metabolic Disease?International journal of molecular sciences · 2024Review
- HOPS, CORVET and newly-identified Hybrid tethering complexes contribute differentially towards multiple modes of endocytosis.Scientific reports · 2023Article
- Article
- Juvenile mucopolysaccharidosis plus disease caused by a missense mutation in VPS33A.Human mutation · 2022Article
- Mucopolysaccharidosis-Plus Syndrome: Report on a Polish Patient with a NovelInternational journal of molecular sciences · 2022Article
Corrections and comments
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Authors and funding
15 authors at 2 institutions in 2 countries.
Funding
Abstract
Mucopolysaccharidoses (MPS) are rare lysosomal storage disorders (LSD) characterized by the excessive accumulation of glycosaminoglycans (GAG). Conventional MPS, caused by inborn deficiencies of lysosomal enzymes involved in GAG degradation, display various multisystemic symptoms-including progressive neurological complications, ophthalmological disorders, hearing loss, gastrointestinal and hepatobiliary issues, cardiorespiratory problems, bone and joint abnormalities, dwarfism, and coarse facial features. Mucopolysaccharidosis-Plus Syndrome (MPSPS), an autosomal recessive disease caused by a mutation in the endo-lysosomal tethering protein VPS33A, shows additional renal and hematopoietic abnormalities ("Plus symptoms") uncommon in conventional MPS. Here, we analyze data from biochemical, histological, and physical examinations-particularly of blood counts and kidney function-to further characterize the clinical phenotype of MPSPS. A series of blood tests indicate hematopoietic symptoms including progressive anemia and thrombocytopenia, which correlate with histological observations of hypoplastic bone marrow. High urinary excretion of protein (caused by impairments in renal filtration), hypoalbuminemia, and elevated levels of creatinine, cholesterol, and uric acid indicate renal dysfunction. Histological analyses of MPSPS kidneys similarly suggest the extensive destruction of glomerular structures by foamy podocytes. Height and weight did not significantly deviate from the average, but in some cases, growth began to decline at around six months or one year of age.
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