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acanthocheilonemiasis/protéinurie
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Transforming growth factor-beta in renal disease with glycogen storage disease I.
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We report a 14-year-old patient with Japanese glycogen storage disease I (GSD-I) who was found to have proteinuria. Renal biopsy revealed massive tubular atrophy and interstitial fibrosis with mononuclear cell infiltration, but the glomeruli were almost normal. The epithelial cells of tubules
Glucose-6-phosphatase deficiency.
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Glucose-6-phosphatase deficiency (G6P deficiency), or glycogen storage disease type I (GSDI), is a group of inherited metabolic diseases, including types Ia and Ib, characterized by poor tolerance to fasting, growth retardation and hepatomegaly resulting from accumulation of glycogen and fat in the
Ramipril treatment in a patient with glycogen storage disease I non-A.
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We studied the effect of ramipril on proteinuria and mild hypertension in a 21-year-old patient affected by glycogen storage disease type I non-A. After few months of therapy we obtained a decrease in total urine protein excretion that later re-increased in spite of the high dose of ACE inhibitor.
Effective renal plasma flow in patients with glycogen storage disease type I.
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To evaluate effective renal plasma flow (ERPF) we performed renal scintigraphies with 99mTc-Mercaptoacetyl-triglycine (MAG3) in nine patients with glycogen storage disease I (GSD I) (age: 16 +/- 7 years). Two patients presented with proteinuria, none showed hyperaminoaciduria, disturbed tubular
Renal histology in two adult patients with type I glycogen storage disease.
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Two adult patients with type I glycogen storage disease (I-GSD) had chronic renal disease with heavy proteinuria. Renal biopsies showed focal glomerular sclerosis, interstitial fibrosis, tubular atrophy or vacuolation, and prominent arteriosclerosis. Marked glomerular hypertrophy was demonstrated
Early diagnosis and treatment may prevent the development of complications in an adult patient with glycogen storage disease type Ia.
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Type Iota(a) glycogen storage disease (GSD Iota(a)) is caused by the deficiency of glucose-6-phosphatase activity, which results in metabolic disorder and organ failure, including renal failure. GSD Iota(a) patients are generally diagnosed at a median age of 6 months. However, we report a
Type I glycogen storage disease: kidney involvement, pathogenesis and its treatment.
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Type I glycogen storage disease (GSD-I) is due to the deficiency of glucose-6-phosphatase activity in the liver, kidney and intestine. Although kidney enlargement occurs in GSD-I, renal disease has not been considered a major problem until recently. In older patients (more than 20 years of age)
Glomerular and tubular function in glycogen storage disease.
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Urinary protein and calcium excretion were assessed in 77 patients with the hepatic glycogen storage diseases (GSD): 30 with GSD-I (median age 12.4 years, range 3.2-32.9 years), 25 with GSD-III (median age 10.5 years, range 4.2-31.3 years) and 22 with GSD-IX (median age 11.8 years, range 1.2-35.4
Hepatorenal correction in murine glycogen storage disease type I with a double-stranded adeno-associated virus vector.
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Glycogen storage disease type Ia (GSD-Ia) is caused by the deficiency of glucose-6-phosphatase (G6Pase). Long-term complications of GSD-Ia include life-threatening hypoglycemia and proteinuria progressing to renal failure. A double-stranded (ds) adeno-associated virus serotype 2 (AAV2) vector
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