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Genetic Disorders Resulting in Hyper- or Hypouricemia

The result's identifiers

  • Result code in IS VaVaI

    <a href="https://www.isvavai.cz/riv?ss=detail&h=RIV%2F00064165%3A_____%2F12%3A13345" target="_blank" >RIV/00064165:_____/12:13345 - isvavai.cz</a>

  • Alternative codes found

    RIV/00216208:11110/12:13345

  • Result on the web

    <a href="http://dx.doi.org/10.1053/j.ackd.2012.06.002" target="_blank" >http://dx.doi.org/10.1053/j.ackd.2012.06.002</a>

  • DOI - Digital Object Identifier

Alternative languages

  • Result language

    angličtina

  • Original language name

    Genetic Disorders Resulting in Hyper- or Hypouricemia

  • Original language description

    Serum uric acid concentrations are governed by the balance of urate production and excretion. Besides well-known secondary causes of hyperuricemia, such as myeloproliferative diseases, decreased renal function, and excessive dietary purine intake, thereare a number of genetic disorders that result in hyper- or hypouricemia. Renal impairment in these disorders may be associated with the development of chronic kidney disease, acute kidney injury, or urate nephrolithiasis. These conditions are frequentlymisdiagnosed, not because the diagnosis is complicated and difficult to ascertain, but rather because of a lack of awareness of the particular condition. The first important step in the diagnosis is obtaining a detailed family history, with evaluation ofserum and urinary urate concentrations. This review will aid physicians in identifying these inherited kidney disorders associated with hyperuricemia and hypouricemia. Identification of these conditions will help to explain the pathogene

  • Czech name

  • Czech description

Classification

  • Type

    J<sub>x</sub> - Unclassified - Peer-reviewed scientific article (Jimp, Jsc and Jost)

  • CEP classification

    EB - Genetics and molecular biology

  • OECD FORD branch

Result continuities

  • Project

    <a href="/en/project/NT11322" target="_blank" >NT11322: Functional characterization of SLC22A12 and SLC2A9 allelic variants in Czech population</a><br>

  • Continuities

    I - Institucionalni podpora na dlouhodoby koncepcni rozvoj vyzkumne organizace

Others

  • Publication year

    2012

  • Confidentiality

    S - Úplné a pravdivé údaje o projektu nepodléhají ochraně podle zvláštních právních předpisů

Data specific for result type

  • Name of the periodical

    Advances in Chronic Kidney Disease

  • ISSN

    1548-5595

  • e-ISSN

  • Volume of the periodical

    19

  • Issue of the periodical within the volume

    6

  • Country of publishing house

    US - UNITED STATES

  • Number of pages

    6

  • Pages from-to

    398-403

  • UT code for WoS article

    000310823000008

  • EID of the result in the Scopus database