ArticlePediatric nephrology (Berlin, Germany)2002
Genetic analysis--a diagnostic tool for primary hyperoxaluria type I.
Article in Pediatric nephrology (Berlin, Germany), 2002. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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Who cites it
7 citing papers in PubMed, 29 citations in OpenAlex.
- Age-Specific Excretion of Calcium, Oxalate, Citrate, and Glycosaminoglycans and Their Ratios in Healthy Children and Children with Urolithiasis.Biomolecules · 2021Article
- Recurrent primary hyperoxaluria type 2 leads to early post-transplant renal function loss: A case report.Experimental and therapeutic medicine · 2018Article
- Late diagnosis of primary hyperoxaluria after failed kidney transplantation.International urology and nephrology · 2010Article
- An overview of the role of genotyping in the diagnosis of the primary hyperoxalurias.Urological research · 2005Review
- Primary hyperoxaluria type 1: is genotyping clinically helpful?Pediatric nephrology (Berlin, Germany) · 2005Review
- Primary hyperoxaluria: liver biopsy or DNA analysis?Pediatric nephrology (Berlin, Germany) · 2003Article
- Recurrent truncating mutations in alanine-glyoxylate aminotransferase gene in two South Indian families with primary hyperoxaluria type 1 causing later onset end-stage kidney disease.Indian journal of nephrologyArticle
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4 authors at 2 institutions in 2 countries.
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No grant is acknowledged in the PubMed record.
Abstract
Primary hyperoxaluria type I is an autosomal recessive metabolic disease in which excessive oxalates are formed by the liver and excreted by the kidneys, causing a wide spectrum of disease, ranging from renal failure in infancy to mere renal stones in late adulthood. The diagnosis may be suspected when clinical signs and increased urinary oxalate and glycolate excretion present, and is confirmed by the measurement of decreased alanine:glyoxylate aminotransferase activity in a liver sample. The enzymatic assay is not readily available to pediatric nephrologists in many parts of the world. We describe three families from Croatia in whom the diagnosis of primary hyperoxaluria was solely based on clinical findings that included nephrolithiasis and nephrocalcinosis accompanied by increased urinary oxalates and glycolate excretion, as enzymatic assays of liver samples could not be performed. Mutation analysis of the AGXT gene encoding the defective enzyme confirmed the diagnosis, revealing three alleles carrying the C156ins mutation and two the G630A mutation. Screening first-degree relatives for the relevant mutation disclosed an asymptomatic affected sibling. Mutation analysis of the AGXT gene is a non-invasive and accurate tool for the diagnosis of type I primary hyperoxaluria that may replace enzymatic assays of liver biopsies.
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