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Hyperuricemia contributes to the faster progression of diabetic kidney disease in type 2 diabetes mellitus

The result's identifiers

  • Result code in IS VaVaI

    <a href="https://www.isvavai.cz/riv?ss=detail&h=RIV%2F00159816%3A_____%2F16%3A00065336" target="_blank" >RIV/00159816:_____/16:00065336 - isvavai.cz</a>

  • Alternative codes found

    RIV/65269705:_____/16:00065336 RIV/00216224:14110/16:00088861

  • Result on the web

    <a href="http://dx.doi.org/10.1016/j.jdiacomp.2016.06.002" target="_blank" >http://dx.doi.org/10.1016/j.jdiacomp.2016.06.002</a>

  • DOI - Digital Object Identifier

    <a href="http://dx.doi.org/10.1016/j.jdiacomp.2016.06.002" target="_blank" >10.1016/j.jdiacomp.2016.06.002</a>

Alternative languages

  • Result language

    angličtina

  • Original language name

    Hyperuricemia contributes to the faster progression of diabetic kidney disease in type 2 diabetes mellitus

  • Original language description

    Aims The aims of the study were (i) to ascertain prognostic value of serum uric acid (SUA) for diabetic kidney disease (DKD) progression and major adverse cardiovascular event (MACE) in a cohort of T2DM patients, (ii) to ascertain eventual protective effect of allopurinol treatment, (iii) to determine the effect of genetic variability in UA transporters on DKD progression, and (iv) to define optimal cut-off values for SUA in patients with DKD. Methods Study comprised 422 subjects with diabetes duration at least 15 years followed-up for a median of 43 [IQR 22-77] months. Participants were categorized into stable or progressors according to their change in albuminuria or chronic kidney disease (CKD) stage. At baseline, 68% patients had hyperuricemia (SUA GREATER-THAN OR EQUAL TO 420 μmol/l for men and GREATER-THAN OR EQUAL TO 360 μmol/l for women and/or allopurinol treatment). Five SNPs in the SLC2A9 and ABCG2 genes were determined by PCR. Results Time-to-event analysis with subgroups defined by the presence/absence of initial hyperuricemia revealed significant differences in all three end-points (P < 0.0001 for DKD progression, P = 0.0022 for MACE and P = 0.0002 for death, log-rank test). Subjects with normal SUA not requiring allopurinol had median time to DKD progression 49 months compared with remaining subjects (32 months, P = 0.0002, log-rank test). Multivariate Cox regression model revealed hyperuricemia (i.e. high SUA and/or allopurinol treatment) significant predictor of DKD progression independent of baseline CKD stage. Optimal cut-off values identified by ROC analysis for T2DM subjects were LESS-THAN OR EQUAL TO 377.5 μmol/l for men and LESS-THAN OR EQUAL TO 309.0 μmol/l for women. We found no differences in allele or genotype frequencies in selected SNPs between patients with and without hyperuricemia (all P > 0.05).

  • Czech name

  • Czech description

Classification

  • Type

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

  • CEP classification

    FE - Other fields of internal medicine

  • OECD FORD branch

Result continuities

  • Project

    <a href="/en/project/NT13198" target="_blank" >NT13198: Pentose phosphate pathway as a potentially new therapeutic target in prevention of diabetic complications</a><br>

  • Continuities

    I - Institucionalni podpora na dlouhodoby koncepcni rozvoj vyzkumne organizace

Others

  • Publication year

    2016

  • Confidentiality

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

Data specific for result type

  • Name of the periodical

    Journal of diabetes and its complications

  • ISSN

    1056-8727

  • e-ISSN

  • Volume of the periodical

    30

  • Issue of the periodical within the volume

    7

  • Country of publishing house

    US - UNITED STATES

  • Number of pages

    8

  • Pages from-to

    1300-1307

  • UT code for WoS article

    000382097600016

  • EID of the result in the Scopus database