ADMA, C-reactive protein, and albuminuria in untreated essential hypertension: a cross-sectional study.
BACKGROUND
Asymmetric dimethylarginine (ADMA) and subclinical inflammation are associated with atherosclerosis progression, whereas microalbuminuria is an established index of hypertensive organ damage.


METHODS
Cross-sectional.


METHODS
In an outpatient hypertensive unit, 296 nondiabetic and untreated participants with hypertension were studied. Participants with atherosclerotic cardiovascular disease, severe valvulopathy, congestive heart failure, presence of neoplastic or other concurrent systemic disease, atrial fibrillation, serum creatinine level > 1.5 mg/dL in men and > 1.4 mg/dL in women, and urinary albumin excretion > 300 mg/24 h were excluded.


METHODS
ADMA and high-sensitivity C-reactive protein (hs-CRP) levels.


METHODS
Albuminuria assessed using albumin-creatinine ratio (ACR).


METHODS
Participants underwent ambulatory blood pressure monitoring, echocardiography, routine assessment of metabolic profile, ADMA, and hs-CRP, whereas ACR was determined as the mean of 3 values in nonconsecutive morning spot urine samples.


RESULTS
64 participants had an ACR of 30-300 mg/g. Stratification based on ADMA level showed that participants with hypertension in quartile [Q] 4 compared with those in Q3, Q2, and Q1 showed the highest ACRs (53.2 vs 31.2 vs 30.4 vs 16.7 mg/g; P < 0.008 for all). Moreover, stratification based on hs-CRP level showed that participants with hypertension in Q4 (69.8% had microalbuminuria) showed the highest ACRs (72.2 vs 25.6, 16.2, and 19.2 mg/g for Q3, Q2, and Q1, respectively; P < 0.008 for all). Stepwise regression analysis showed that age, 24-hour systolic blood pressure, hs-CRP level, ADMA level, and the interaction of hs-CRP with ADMA were independent predictors of ACR (R(2) = 0.674; P < 0.001).


CONCLUSIONS
Cross-sectional study.


CONCLUSIONS
In patients with untreated essential hypertension, increased hs-CRP and ADMA levels are associated with microalbuminuria, suggesting the involvement of inflammation and endothelial dysfunction in vascular and kidney damage.
Tsioufis
Costas
C
First Cardiology Clinic, University of Athens, Hippokration Hospital, Athens, Greece. ktsioufis@hippocratio.gr
Dimitriadis
Kyriakos
K
Andrikou
Eirini
E
Thomopoulos
Costas
C
Tsiachris
Dimitris
D
Stefanadi
Elli
E
Mihas
Costas
C
Miliou
Antigoni
A
Papademetriou
Vassilios
V
Stefanadis
Christodoulos
C
D000328:Adult; D000419:Albuminuria / Q000378:metabolism* / Q000503:physiopathology; D001120:Arginine / Q000031:analogs & derivatives* / Q000378:metabolism; D001794:Blood Pressure / Q000502:physiology; D002097:C-Reactive Protein / Q000378:metabolism*; D003404:Creatinine / Q000378:metabolism; D003430:Cross-Sectional Studies; D004730:Endothelium, Vascular / Q000503:physiopathology; D005260:Female; D006801:Humans; D006973:Hypertension / Q000378:metabolism* / Q000503:physiopathology; D007249:Inflammation / Q000503:physiopathology; D008297:Male; D008875:Middle Aged; D012044:Regression Analysis; D012709:Serum Albumin / Q000378:metabolism
D012709:Serum Albumin; C018524:N,N-dimethylarginine; D002097:C-Reactive Protein; D001120:Arginine; D003404:Creatinine