title: Pentraxin 3 as a novel bio-marker of inflammation and endothelial dysfunction in autosomal dominant polycystic kidney disease.
abstract: OBJECTIVE
  Cardiovascular disease (CVD) is the main cause of mortality in patients with autosomal dominant polycystic kidney disease (ADPKD). Prior to hypertension early vascular changes and inflammation have been reported. We aimed to investigate long pentraxin 3 (PTX-3), which has been recently described as a biomarker of inflammation, and its relation with endothelial dysfunction in early ADPKD patients.
  
  
  METHODS
  Twenty-five ADPKD patients without hypertension and 25 healthy controls were studied cross-sectionally. Hypertension was diagnosed with ambulatory blood pressure monitoring. Plasma concentrations of PTX-3 and proteinuria levels were obtained from each participant. Endothelial dysfunction was assessed using ischemia-induced forearm flow-mediated vasodilation (FMD).
  
  
  RESULTS
  PTX-3 levels were higher in ADPKD patients compared to healthy controls (4.2 [1.2-10.1] vs. 1.4 [0.4-3.1] ng/ml, p < 0.001). Additionally, C-reactive protein (CRP) and proteinuria levels were higher in ADPKD patients than in healthy subjects. In the whole cohort, PTX-3 correlated negatively with FMD (r: -0.58, p < 0.001) and positively with proteinuria (r: 0.56, p < 0.001) and uric acid (r: 0.57, p < 0.001). In all subjects, FMD was independently predicted by PTX-3, but not by uric acid, CRP or proteinuria.
  
  
  CONCLUSIONS
  PTX-3 may be a better biomarker of inflammation than CRP to predict endothelial dysfunction in normotensive ADPKD patients with well-preserved kidney function. Hence, inflammation which is demonstrated by PTX-3 may potentially be used to predict future CVD in this population.
authors: Department of Nephrology, Erciyes University Medical Faculty, 38039, Kayseri, Turkey, iikocyigit@gmail.com.
authors: Ismail
authors: I
authors: Kocyigit
authors: Eray
authors: E
authors: Eroglu
authors: Ozcan
authors: O
authors: Orscelik
authors: Aydin
authors: A
authors: Unal
authors: Ozkan
authors: O
authors: Gungor
authors: Fahir
authors: F
authors: Ozturk
authors: Cigdem
authors: C
authors: Karakukcu
authors: Hakan
authors: H
authors: Imamoglu
authors: Murat Hayri
authors: MH
authors: Sipahioglu
authors: Bulent
authors: B
authors: Tokgoz
authors: Oktay
authors: O
authors: Oymak
mesh_terms: D000328:Adult; D015415:Biomarkers / Q000097:blood; D002097:C-Reactive Protein / Q000378:metabolism*; D016022:Case-Control Studies; D003430:Cross-Sectional Studies; D004730:Endothelium, Vascular / Q000503:physiopathology*; D005260:Female; D006801:Humans; D007249:Inflammation / Q000097:blood; D008297:Male; D008875:Middle Aged; D016891:Polycystic Kidney, Autosomal Dominant / Q000097:blood* / Q000652:urine; D011507:Proteinuria / Q000209:etiology; D000683:Serum Amyloid P-Component / Q000378:metabolism*; D014527:Uric Acid / Q000097:blood; D014664:Vasodilation; D000099153:Pentraxins
chemical_list: D015415:Biomarkers; D002097:C-Reactive Protein; D000683:Serum Amyloid P-Component; D014527:Uric Acid; D000099153:Pentraxins