title: Pentraxin 3 as a new indicator of cardiovascular‑related death in patients with advanced chronic kidney disease.
abstract: INTRODUCTION    Pentraxin3 (PTX3) play an important role in the inflammatory response, taking part in recognizing pathogens and damaged tissues. OBJECTIVES    The aim of the study was to assess the relationship between PTX3 levels and all-cause and cardiovascular (CV) mortality in chronic kidney disease (CKD) patients during five-year observation period.  PATIENTS AND METHODS    The study comprised 78 patients (51 hemodialyzed, 27 predialysis). The examined parameters included PTX3, calcium, phosphate, iPTH, interleukin-6 (IL-6), fibroblast growth factor 23 (FGF-23), osteopontin (OPN), osteoprotegerin (OPG), osteocalcin (OC), osteopontin (OPN), osteoprotegerin (OPG), osteocalcin, tumor necrosis factor receptor II (TNF-R II), transforming growth factor-β (TGF-β), hepatocyte growth factor (HGF), stromal cell-derived factor α (SDF1α), and thrombomodulin (TM). In a subgroup of 45 patients, fragments of radial artery obtained during creation of hemodialysis access were stained for calcifications. In 51 patients, ultrasonography was performed to assess intima-media thickness (CCA-IMT).  RESULTS    Median serum concentration of PTX3 was 1.43 (0.74-2.50) ng/ml. Higher concentrations of fibrinogen, CRP, IL-6, TNF-R II, TGFβ1, HGF, OPN, OPG, FGF-23, TM, SDF1α, lower albumin and uric acid levels were observed in patients with PTX3 above the median. During follow-up, 27 patients (35%) died, including 25 due to CV causes. In contrast to CRP, baseline PTX3 predicted CV mortality independently of classical CV risk factors. Also, PTX3 concentrations significantly predicted mortality after adjustment for age, baseline dialysis status, serum OPG and CRP, radial artery calcifications, and CCA-IMT. CONCLUSIONS    We postulate that PTX3 might be an early marker of CV mortality in patients with advanced CKD yet before the increase of specific marker for systemic inflammation like hsCRP.
authors.forename: Marcin
authors.initials: M
authors.lastname: Krzanowski
authors.forename: Katarzyna
authors.initials: K
authors.lastname: Krzanowska
authors.forename: Mariusz
authors.initials: M
authors.lastname: Gajda
authors.forename: Paulina
authors.initials: P
authors.lastname: Dumnicka
authors.forename: Artur
authors.initials: A
authors.lastname: Dziewierz
authors.forename: Karolina
authors.initials: K
authors.lastname: Woziwodzka
authors.forename: Jan A
authors.initials: JA
authors.lastname: Litwin
authors.forename: Władysław
authors.initials: W
authors.lastname: Sułowicz
mesh_terms: D000328:Adult; D000368:Aged; D015415:Biomarkers / Q000097:blood; D002097:C-Reactive Protein / Q000032:analysis*; D002318:Cardiovascular Diseases / Q000097:blood* / Q000175:diagnosis / Q000209:etiology / Q000401:mortality; D059168:Carotid Intima-Media Thickness; D005260:Female; D000089703:Fibroblast Growth Factor-23; D006801:Humans; D007249:Inflammation; D008297:Male; D008875:Middle Aged; D011379:Prognosis; D051436:Renal Insufficiency, Chronic / Q000150:complications*; D012307:Risk Factors; D000683:Serum Amyloid P-Component / Q000032:analysis*; D000099153:Pentraxins
chemical_list: D015415:Biomarkers; D002097:C-Reactive Protein; D000089703:Fibroblast Growth Factor-23; D000683:Serum Amyloid P-Component; D000099153:Pentraxins; C000717427:FGF23 protein, human