• Je něco špatně v tomto záznamu ?

The Impact of Blood Pressure and Visceral Adiposity on the Association of Serum Uric Acid With Albuminuria in Adults Without Full Metabolic Syndrome

A. Krajcoviechova, J. Tremblay, P. Wohlfahrt, J. Bruthans, MR. Tahir, P. Hamet, R. Cifkova,

. 2016 ; 29 (12) : 1335-1342.

Jazyk angličtina Země Spojené státy americké

Typ dokumentu časopisecké články

Perzistentní odkaz   https://www.medvik.cz/link/bmc18017077

Grantová podpora
NV15-27109A MZ0 CEP - Centrální evidence projektů

BACKGROUND: The impact of metabolic phenotypes on the association of uricemia with urinary albumin/creatinine ratio (uACR) remains unresolved. We evaluated the association between serum uric acid and uACR in persons with 0, and 1-2 metabolic syndrome (MetS) components and determined the modification effects of visceral adiposity index (VAI), mean arterial pressure (MAP), and fasting glucose on this association. METHODS: Using data from a cross-sectional survey of a representative Czech population aged 25-64 years (n = 3612), we analyzed 1,832 persons without decreased glomerular filtration rate <60ml/min/1.73 m2, diabetes, and MetS. MetS components were defined using the joint statement of the leading societies. RESULTS: Of the 1,832 selected participants, 64.1% (n = 1174) presented with 1-2 MetS components (age 46.3±11.2; men 51.7%), whereas 35.9% (n = 658) were free of any component (age 39.4±10.0; men 34.2 %). In fully adjusted multiple linear regression models for uricemia, uACR was an independent factor for increase in uric acid levels only in persons with 1-2 MetS components (standardized beta (Sβ) 0.048; P = 0.024); however, not in those without any component (Sβ 0.030; P = 0.264). Uric acid levels increased by the interaction of uACR with VAI (Sβ 0.06; P = 0.012), and of uACR with MAP (Sβ 0.05; P = 0.009). Finally, the association of uACR with uricemia was confined to persons whose VAI together with MAP were ≥the median of 1.35 and 98mm Hg, respectively (Sβ 0.190; P < 0.001). CONCLUSIONS: We demonstrated a strong modification effect of VAI and MAP on the association between uACR and uricemia, which suggests obesity-related hypertension as the underlying mechanism.

Citace poskytuje Crossref.org

000      
00000naa a2200000 a 4500
001      
bmc18017077
003      
CZ-PrNML
005      
20180523111201.0
007      
ta
008      
180515s2016 xxu f 000 0|eng||
009      
AR
024    7_
$a 10.1093/ajh/hpw098 $2 doi
035    __
$a (PubMed)27565787
040    __
$a ABA008 $b cze $d ABA008 $e AACR2
041    0_
$a eng
044    __
$a xxu
100    1_
$a Krajcoviechova, Alena $u Center for Cardiovascular Prevention, First Faculty of Medicine, Charles University in Prague and Thomayer Hospital, Prague, Czech Republic. Montreal University Hospital Research Center, CHUM, Montréal, Canada.
245    14
$a The Impact of Blood Pressure and Visceral Adiposity on the Association of Serum Uric Acid With Albuminuria in Adults Without Full Metabolic Syndrome / $c A. Krajcoviechova, J. Tremblay, P. Wohlfahrt, J. Bruthans, MR. Tahir, P. Hamet, R. Cifkova,
520    9_
$a BACKGROUND: The impact of metabolic phenotypes on the association of uricemia with urinary albumin/creatinine ratio (uACR) remains unresolved. We evaluated the association between serum uric acid and uACR in persons with 0, and 1-2 metabolic syndrome (MetS) components and determined the modification effects of visceral adiposity index (VAI), mean arterial pressure (MAP), and fasting glucose on this association. METHODS: Using data from a cross-sectional survey of a representative Czech population aged 25-64 years (n = 3612), we analyzed 1,832 persons without decreased glomerular filtration rate <60ml/min/1.73 m2, diabetes, and MetS. MetS components were defined using the joint statement of the leading societies. RESULTS: Of the 1,832 selected participants, 64.1% (n = 1174) presented with 1-2 MetS components (age 46.3±11.2; men 51.7%), whereas 35.9% (n = 658) were free of any component (age 39.4±10.0; men 34.2 %). In fully adjusted multiple linear regression models for uricemia, uACR was an independent factor for increase in uric acid levels only in persons with 1-2 MetS components (standardized beta (Sβ) 0.048; P = 0.024); however, not in those without any component (Sβ 0.030; P = 0.264). Uric acid levels increased by the interaction of uACR with VAI (Sβ 0.06; P = 0.012), and of uACR with MAP (Sβ 0.05; P = 0.009). Finally, the association of uACR with uricemia was confined to persons whose VAI together with MAP were ≥the median of 1.35 and 98mm Hg, respectively (Sβ 0.190; P < 0.001). CONCLUSIONS: We demonstrated a strong modification effect of VAI and MAP on the association between uACR and uricemia, which suggests obesity-related hypertension as the underlying mechanism.
650    12
$a adipozita $7 D050154
650    _2
$a dospělí $7 D000328
650    _2
$a albuminurie $x diagnóza $x epidemiologie $x patofyziologie $x moč $7 D000419
650    _2
$a biologické markery $x krev $x moč $7 D015415
650    12
$a krevní tlak $7 D001794
650    _2
$a rozdělení chí kvadrát $7 D016009
650    _2
$a kreatinin $x moč $7 D003404
650    _2
$a průřezové studie $7 D003430
650    _2
$a Česká republika $x epidemiologie $7 D018153
650    _2
$a ženské pohlaví $7 D005260
650    _2
$a hodnoty glomerulární filtrace $7 D005919
650    _2
$a lidé $7 D006801
650    _2
$a hypertenze $x diagnóza $x epidemiologie $x patofyziologie $7 D006973
650    _2
$a hyperurikemie $x krev $x diagnóza $x epidemiologie $7 D033461
650    _2
$a nitrobřišní tuk $x patofyziologie $7 D050152
650    _2
$a ledviny $x patofyziologie $7 D007668
650    _2
$a lineární modely $7 D016014
650    _2
$a mužské pohlaví $7 D008297
650    _2
$a metabolický syndrom $x krev $x diagnóza $x epidemiologie $x patofyziologie $7 D024821
650    _2
$a lidé středního věku $7 D008875
650    _2
$a obezita $x diagnóza $x epidemiologie $x patofyziologie $7 D009765
650    _2
$a fenotyp $7 D010641
650    _2
$a prediktivní hodnota testů $7 D011237
650    _2
$a rizikové faktory $7 D012307
650    _2
$a kyselina močová $x krev $7 D014527
655    _2
$a časopisecké články $7 D016428
700    1_
$a Tremblay, Johanne $u Montreal University Hospital Research Center, CHUM, Montréal, Canada.
700    1_
$a Wohlfahrt, Peter $u Center for Cardiovascular Prevention, First Faculty of Medicine, Charles University in Prague and Thomayer Hospital, Prague, Czech Republic. Department of Preventive Cardiology, Institute for Clinical and Experimental Medicine, Prague, Czech Republic.
700    1_
$a Bruthans, Jan $u Center for Cardiovascular Prevention, First Faculty of Medicine, Charles University in Prague and Thomayer Hospital, Prague, Czech Republic.
700    1_
$a Tahir, Muhmmad Ramzan $u Montreal University Hospital Research Center, CHUM, Montréal, Canada.
700    1_
$a Hamet, Pavel $u Montreal University Hospital Research Center, CHUM, Montréal, Canada.
700    1_
$a Cifkova, Renata $u Center for Cardiovascular Prevention, First Faculty of Medicine, Charles University in Prague and Thomayer Hospital, Prague, Czech Republic.
773    0_
$w MED00000255 $t American journal of hypertension $x 1941-7225 $g Roč. 29, č. 12 (2016), s. 1335-1342
856    41
$u https://pubmed.ncbi.nlm.nih.gov/27565787 $y Pubmed
910    __
$a ABA008 $b sig $c sign $y a $z 0
990    __
$a 20180515 $b ABA008
991    __
$a 20180523111346 $b ABA008
999    __
$a ok $b bmc $g 1300701 $s 1013917
BAS    __
$a 3
BAS    __
$a PreBMC
BMC    __
$a 2016 $b 29 $c 12 $d 1335-1342 $i 1941-7225 $m American journal of hypertension $n Am J Hypertens $x MED00000255
GRA    __
$a NV15-27109A $p MZ0
LZP    __
$a Pubmed-20180515

Najít záznam

Citační ukazatele

Nahrávání dat ...

    Možnosti archivace