Pentraxin 3 as a new indicator of cardiovascular-related death in patients with advanced chronic kidney disease

Pentraxin 3 (PTX3) is involved in inflammatory response by recognizing pathogens and damaged tissues. The aim of this study was to assess the relationship between PTX3 levels and all‑cause and cardiovascular (CV) mortality in patients with chronic kidney disease (CKD) during 5‑year follow‑up. The study included 78 patients (51 on hemodialysis and 27 on predialysis). We measured the levels of PTX3, calcium, phosphate, intact parathyroid hormone, high-sensitivity Creactive protein (hs-CRP), interleukin 6 (IL‑6), fibroblast growth factor 23 (FGF‑23), osteopontin (OPN), osteocalcin (OC), osteoprotegerin (OPG), fetuin A, tumor necrosis factor receptor 2 (TNFR2), transforming growth factor $\beta1$ ($TGF‑\beta 1$), hepatocyte growth factor (HGF), stromal cell‑derived factor $1\alpha$ ($SDF‑1\alpha$), and thrombomodulin (TM). In a subgroup of 45 patients, fragments of the radial artery obtained during creation of hemodialysis access were stained for calcifications. In 51 patients, ultrasonography was performed to assess common carotid artery intima–media thickness (CCA‑IMT). The median serum concentrations of PTX3 were 1.43 ng/ml (interquartile range, 0.74–2.50). Higher concentrations of fibrinogen, hs‑CRP, IL‑6, TNFR2, $TGF‑\beta$ 1, HGF, OPN, OPG, FGF‑23, TM, and $SDF‑1\alpha$ and 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 hs-CRP levels, baseline PTX3 levels predicted CV mortality independently of classic CV risk factors. PTX3 levels also significantly predicted mortality after adjustment for age, baseline dialysis status, serum OPG and CRP levels, radial artery calcifications, and CCA‑IMT. We postulate that PTX3 might be an early marker of CV mortality in patients with advanced CKD, yet before the increase in the levels of a specific marker for systemic inflammation such as hs‑CRP.