Laboratory for Molecular Diagnostics
Center for Nephrology and Metabolic Disorders
The disposition to develop gout disease is hereditary. For type 1, the gene ABCG2 is responsible.
Hyperuricemia
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Gout susceptibility 1
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ABCG2
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Hyperuricemic nephropathy
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Kelley-Seegmiller syndrome
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Lesch-Nyhan syndrome
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| 1. |
Dehghan A et al. (2008) Association of three genetic loci with uric acid concentration and risk of gout: a genome-wide association study. 
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| 2. |
Matsuo H et al. (2009) Common defects of ABCG2, a high-capacity urate exporter, cause gout: a function-based genetic analysis in a Japanese population.
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| 3. |
Martinon F et al. (2006) Gout-associated uric acid crystals activate the NALP3 inflammasome.
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| 4. |
None (1979) Genetics of hyperuricemia in families with gout.
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| 5. |
Healey LA et al. (1967) Hyperuricemia in Filipinos: interaction of heredity and environment.
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| 6. |
HAUGE M et al. (1955) Heredity in gout and hyperuricemia.
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| 7. |
None (1960) Heredity in primary gout.
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| 8. |
NEEL JV et al. (1965) STUDIES ON HYPERURICEMIA. II. A RECONSIDERATION OF THE DISTRIBUTION OF SERUM URIC ACID VALUES IN THE FAMILIES OF SMYTH, COTTERMAN, AND FREYBERG.
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| 9. |
Cheng LS et al. (2004) Genomewide scan for gout in taiwanese aborigines reveals linkage to chromosome 4q25.
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| 10. |
Woodward OM et al. (2011) ABCG transporters and disease.
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| 11. |
Köttgen A et al. (2013) Genome-wide association analyses identify 18 new loci associated with serum urate concentrations.
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| 12. |
OMIM.ORG article Omim 138900
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