Inflammatory status in patients with chronic renal failure: the role of PTX3 and pro-inflammatory cytokines

Int J Mol Med. 2007 Oct;20(4):471-81.

Abstract

Increased plasma levels of several acute phase proteins, such as C-reactive protein (CRP), have been documented among different patients with chronic renal failure (CRF). The aim of the present study was to determine whether pentraxin-3 (PTX3) is a reliable marker of inflammation in CRF. Plasma samples and monocytes were taken from 43 patients before and after undergoing haemodialysis (HD), from 45 uraemic patients (UR) without HD treatment and from 25 healthy controls. Plasma and monocyte samples were analyzed by ELISA for levels of PTX3, tumor necrosis factor-alpha (TNF-alpha), interleukin-1beta (IL-1beta) and interleukin-6 (IL-6); all of these protein levels were higher in CRF patients with respect to the controls. After HD, plasma PTX3 and cytokine levels increased. Inter- and intra-individual variations in CRP were observed in HD patients, while PTX3 plasma levels were stable. Release of PTX3, TNF-alpha, IL-1beta and IL-6 by unstimulated monocytes from patients, before and after HD, was higher with respect to UR patients and controls. After lipopolysaccharide stimulation, all values were higher in patients before HD than those in UR patients, but lower when compared to those in the controls. In contrast, no changes were observed after HD. A significant correlation among plasma PTX3 versus fibrinogen, TNF-alpha and IL-1beta was observed in HD and UR patients. Collectively, these data suggest that PTX3 protein may represent an additional and stable marker of inflammation in CRF.

MeSH terms

  • Aged
  • C-Reactive Protein / metabolism*
  • Cell Separation
  • Cytokines / blood
  • Cytokines / metabolism*
  • Female
  • Fibrinogen / metabolism
  • Humans
  • Inflammation
  • Inflammation Mediators / blood
  • Inflammation Mediators / metabolism*
  • Kidney Failure, Chronic / pathology*
  • Lipopolysaccharides / pharmacology
  • Male
  • Monocytes / drug effects
  • Monocytes / metabolism
  • Renal Dialysis
  • Serum Amyloid P-Component / metabolism*
  • Subcellular Fractions / drug effects
  • Time Factors
  • Uremia / blood

Substances

  • Cytokines
  • Inflammation Mediators
  • Lipopolysaccharides
  • Serum Amyloid P-Component
  • PTX3 protein
  • Fibrinogen
  • C-Reactive Protein