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Hypomagnesaemia is absent in children with autosomal dominant polycystic kidney disease

The result's identifiers

  • Result code in IS VaVaI

    <a href="https://www.isvavai.cz/riv?ss=detail&h=RIV%2F00064203%3A_____%2F19%3A10393810" target="_blank" >RIV/00064203:_____/19:10393810 - isvavai.cz</a>

  • Alternative codes found

    RIV/00216208:11130/19:10393810

  • Result on the web

    <a href="https://verso.is.cuni.cz/pub/verso.fpl?fname=obd_publikace_handle&handle=N98gq959GJ" target="_blank" >https://verso.is.cuni.cz/pub/verso.fpl?fname=obd_publikace_handle&handle=N98gq959GJ</a>

  • DOI - Digital Object Identifier

    <a href="http://dx.doi.org/10.1177/0004563218785190" target="_blank" >10.1177/0004563218785190</a>

Alternative languages

  • Result language

    angličtina

  • Original language name

    Hypomagnesaemia is absent in children with autosomal dominant polycystic kidney disease

  • Original language description

    Background: Hypomagnesaemia is present in 40-50% of children with autosomal dominant renal cysts and diabetes syndrome (RCAD). On the contrary, the prevalence of hypomagnesaemia in children with autosomal dominant polycystic kidney disease (ADPKD) has never been examined. We aimed to investigate whether hypomagnesaemia is present in children with polycystic kidney diseases. Methods: Children with cystic kidney diseases were investigated in a cross-sectional study. Serum concentrations of magnesium (S-Mg) and fractional excretion of magnesium (FE-Mg) were tested. Fifty-four children with ADPKD (n = 26), autosomal recessive polycystic kidney disease (ARPKD) (n = 16) and RCAD (n = 12) with median age of 11.2 (0.6-18.6) years were investigated. Results: Hypomagnesaemia (S-Mg &lt; 0.7 mmol/L) was detected in none of the children with ADPKD/ARPKD and in eight children (67%) with RCAD. Median S-Mg in children with ADPKD/ARPKD was significantly higher than in children with RCAD (0.89 vs. 0.65 mmol/L, P &lt; 0.01). The FE-Mg was increased in 23% of patients with ADPKD/ARPKD (all had chronic kidney disease stages 2-4) and in 63% of patients with RCAD, where it significantly correlated with estimated glomerular filtration rate (r = -0.87, P &lt; 0.01). Conclusions: Hypomagnesaemia is absent in children with ADPKD or ARPKD and could serve as a marker for differential diagnostics between ADPKD, ARPKD and RCAD in children with cystic kidney diseases of unknown origin where molecular genetic testing is lacking. However, while hypomagnesaemia, in the absence of diuretics, appears to rule out ADPKD and ARPKD, normomagnesaemia does not rule out RCAD at least in those aged &lt;3 years.

  • Czech name

  • Czech description

Classification

  • Type

    J<sub>imp</sub> - Article in a specialist periodical, which is included in the Web of Science database

  • CEP classification

  • OECD FORD branch

    30209 - Paediatrics

Result continuities

  • Project

    <a href="/en/project/NT11457" target="_blank" >NT11457: Multigenic etiology in hereditary kidney disorders in children: polycystic kidney disease and atypical HUS</a><br>

  • Continuities

    P - Projekt vyzkumu a vyvoje financovany z verejnych zdroju (s odkazem do CEP)<br>I - Institucionalni podpora na dlouhodoby koncepcni rozvoj vyzkumne organizace

Others

  • Publication year

    2019

  • Confidentiality

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

Data specific for result type

  • Name of the periodical

    Annals of Clinical Biochemistry

  • ISSN

    0004-5632

  • e-ISSN

  • Volume of the periodical

    56

  • Issue of the periodical within the volume

    1

  • Country of publishing house

    GB - UNITED KINGDOM

  • Number of pages

    5

  • Pages from-to

    90-94

  • UT code for WoS article

    000454148900011

  • EID of the result in the Scopus database

    2-s2.0-85049867862