title: The relationship between asymptomatic organ damage, and serum soluble tumor necrosis factor-like weak inducer of apoptosis (sTWEAK) and Interleukin-17A (IL-17A) levels in non-diabetic hypertensive patients.
abstract: BACKGROUND
  This study aimed to measure the serum soluble tumor necrosis factor-like weak inducer of apoptosis (sTWEAK) and interleukin-17A (IL-17A) levels in hypertensive patients with/without asymptomatic organ damage (AOD), as well as to determine the relationship between the serum sTWEAK and IL17-A levels, and carotid intima media thickness (CIMT), proteinuria, retinopathy, and the left ventricle mass index (LVMI).
  
  
  METHODS
  The study included 159 patients diagnosed with and followed-up for primary hypertension (HT); 79 of the patients had AOD (61 female and 18 male) and 80 did not (52 female and 28 male). sTWEAK and IL-17A levels were measured in all patients.
  
  
  RESULTS
  The sTWEAK level was significantly lower in the patients with AOD than in those without AOD (858.4 pg/mL vs. 1151.58 pg/mL, P = 0.001). The sTWEAK level was negatively correlated with the mean microalbuminuria level and LVMI. The median IL-17A level was significantly higher in the patients with AOD than in those without AOD (2.34 pg/mL vs. 1.80 pg/mL, P = 0.001). There was a positive correlation between mean IL-17A level, and mean microalbuminuria level, CIMT, and LVMI. Multivariate logistic regression analysis showed that patient age, sTWEAK level, and mean 24-h systolic blood pressure were predictors of AOD.
  
  
  CONCLUSIONS
  The sTWEAK level was lower and IL-17A level was higher in the patients with AOD. It remains unknown if sTWEAK and IL-17A play a role in the pathophysiology of AOD. Prospective observational studies are needed to determine the precise role of sTWEAK and IL-17A in the development of target organ damage.
authors.affiliation: Department of Nephrology, Ankara Numune Education and Research Hospital, Sıhhiye, Ankara 061100, Turkey. dr.ihsanates@hotmail.com.
authors.forename: Ihsan
authors.initials: I
authors.lastname: Ates
authors.forename: Nihal
authors.initials: N
authors.lastname: Ozkayar
authors.forename: Fatma
authors.initials: F
authors.lastname: Akyel
authors.forename: Canan
authors.initials: C
authors.lastname: Topcuoglu
authors.forename: Serdar
authors.initials: S
authors.lastname: Akyel
authors.forename: A Nurdan
authors.initials: AN
authors.lastname: Barça
authors.forename: Fatih
authors.initials: F
authors.lastname: Dede
mesh_terms: D000328:Adult; D000368:Aged; D000419:Albuminuria / Q000097:blood / Q000209:etiology; D000959:Antihypertensive Agents / Q000627:therapeutic use; D058070:Asymptomatic Diseases; D059168:Carotid Intima-Media Thickness; D000074049:Cytokine TWEAK; D003971:Diastole; D018450:Disease Progression; D005260:Female; D006801:Humans; D006973:Hypertension / Q000097:blood* / Q000150:complications / Q000188:drug therapy; D058437:Hypertensive Retinopathy / Q000097:blood / Q000209:etiology; D017379:Hypertrophy, Left Ventricular / Q000097:blood / Q000209:etiology; D020381:Interleukin-17 / Q000097:blood*; D008297:Male; D008875:Middle Aged; D009929:Organ Size; D012372:ROC Curve; D012307:Risk Factors; D013599:Systole; D048069:Tumor Necrosis Factors / Q000097:blood*
chemical_list: D000959:Antihypertensive Agents; D000074049:Cytokine TWEAK; C508717:IL17A protein, human; D020381:Interleukin-17; C109743:TNFSF12 protein, human; D048069:Tumor Necrosis Factors