Association of tumor necrosis factor-alpha with early target organ damage in newly diagnosed patients with essential hypertension.
OBJECTIVE
To investigate the relationship between inflammatory parameters [high-sensitivity C-reactive protein (hs-CRP), serum tumor necrosis factor-alpha (TNF-alpha) and urinary TNF-alpha] with subclinical cardiac and renal markers of early target organ damage (TOD) in essential hypertension.


METHODS
Preclinical TOD [left ventricular hypertrophy (LVH) and microalbuminuria (MAB)] was evaluated in 40 newly diagnosed never-treated patients with essential hypertension. Serum and urinary TNF-alpha and hs-CRP were measured as inflammatory parameters. Twenty-one BMI-matched and sex-matched normotensive, healthy individuals were included as control group.


RESULTS
The serum levels of hs-CRP and the urinary TNF-alpha excretion were higher in hypertensive patients with MAB, whereas patients with LVH presented higher levels of urinary TNF-alpha. The only difference between hypertensive patients without TOD and healthy controls was the higher urinary excretion of TNF-alpha. Partial correlation analysis showed a significant association between urinary albumin excretion (UAE) and systolic blood pressure (r=0.62, P<0.0001), hs-CRP (r=0.64, P<0.001), urinary TNF-alpha (r=0.55, P=0.001) and Cornell product (r=0.33, P<0.05), whereas the Cornell product was related to UAE (r=0.34, P<0.05), urinary TNF-alpha (r=0.45, P<0.01), and hs-CRP (r=0.32, P<0.05). Multiple regression analysis demonstrated that the parameters independently correlated with UAE were mean blood pressure, Cornell product, hs-CRP and urinary TNF-alpha (adjusted R2=0.77, P<0.001), whereas UAE, urinary TNF-alpha and hs-CRP were independently correlated with Cornell product (adjusted R2=0.66, P<0.001). Multiple logistic regression analysis with TOD as the dependent variable showed that hs-CRP [2.24 (1.17-4.28), P<0.05] and urinary TNF-alpha [1.21 (1.02-1.44), P<0.05] were independently related to TOD.


CONCLUSIONS
Urinary TNF-alpha is independently correlated with UAE and Cornell product in essential hypertension, suggesting that inflammation may participate in the development of TOD. In addition, urinary excretion of TNF-alpha might be an early marker of preclinical TOD in hypertensive patients. Finally, these results may be a basis to study the effect of the blockade of TNF-alpha activity on the development and progression of TOD in essential hypertension.
Navarro-González
Juan F
JF
Nephrology Service, University Hospital Nuestra Señora de Candelaria, Santa Cruz de Tenerife, Spain. jnavgon@gobiernodecanarias.eorg
Mora
Carmen
C
Muros
Mercedes
M
Jarque
Ana
A
Herrera
Haridian
H
García
Javier
J
D000419:Albuminuria / Q000378:metabolism*; D001794:Blood Pressure; D002097:C-Reactive Protein / Q000032:analysis*; D003430:Cross-Sectional Studies; D005260:Female; D006801:Humans; D006973:Hypertension / Q000150:complications / Q000378:metabolism*; D017379:Hypertrophy, Left Ventricular / Q000209:etiology / Q000378:metabolism*; D007674:Kidney Diseases / Q000209:etiology / Q000378:metabolism*; D008297:Male; D008875:Middle Aged; D014409:Tumor Necrosis Factor-alpha / Q000032:analysis*
D014409:Tumor Necrosis Factor-alpha; D002097:C-Reactive Protein