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

Identifikátory výsledku

  • Kód výsledku v 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>

  • Nalezeny alternativní kódy

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

  • Výsledek na webu

    <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>

Alternativní jazyky

  • Jazyk výsledku

    angličtina

  • Název v původním jazyce

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

  • Popis výsledku v původním jazyce

    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).

  • Název v anglickém jazyce

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

  • Popis výsledku anglicky

    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).

Klasifikace

  • Druh

    J<sub>x</sub> - Nezařazeno - Článek v odborném periodiku (Jimp, Jsc a Jost)

  • CEP obor

    FE - Ostatní obory vnitřního lékařství

  • OECD FORD obor

Návaznosti výsledku

  • Projekt

    <a href="/cs/project/NT13198" target="_blank" >NT13198: Pentózový cyklus jako potenciální nový terapeutický cíl v prevenci diabetických komplikací</a><br>

  • Návaznosti

    I - Institucionalni podpora na dlouhodoby koncepcni rozvoj vyzkumne organizace

Ostatní

  • Rok uplatnění

    2016

  • Kód důvěrnosti údajů

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

Údaje specifické pro druh výsledku

  • Název periodika

    Journal of diabetes and its complications

  • ISSN

    1056-8727

  • e-ISSN

  • Svazek periodika

    30

  • Číslo periodika v rámci svazku

    7

  • Stát vydavatele periodika

    US - Spojené státy americké

  • Počet stran výsledku

    8

  • Strana od-do

    1300-1307

  • Kód UT WoS článku

    000382097600016

  • EID výsledku v databázi Scopus