title: Relationship among endothelial response to hyperemia, bone marrow-derived progenitor cells, and parathyroid hormone in renal transplantation.
abstract: BACKGROUND
  Endothelial dysfunction may contribute to modulate cardiovascular complications in renal transplant recipients (RTRs), and a relationship between endothelial dysfunction and parathyroid hormone (PTH) levels in RTRs has been demonstrated. We evaluated the relationship between endothelial response to hyperemia and circulating progenitor cells (CPCs) and endothelial progenitor cells (EPCs) PTH, and genetic parameters in RTRs.
  
  
  METHODS
  In 120 RTRs and in healthy subjects without (n=107, group A) and with cardiovascular risk factors (n=109, group B), we evaluated endothelial response to hyperemia through digital tonometry (peripheral arterial tonometry) detected by reactive hyperemia index (RHI) and EPCs and CPCs by flow cytometry.
  
  
  RESULTS
  In RTRs, RHI median value was lower than in group A (P=0.05). EPC number was significantly lower in RTRs than in groups A and B (P<0.0001), whereas PTH median value was significantly higher (P<0.0001). In RTRs, RHI values were significantly lower according to the presence of three or more risk factors (P=0.04) and positively correlated with EPCs (P=0.04) but not with PTH (P=0.2). In patients who underwent dialysis for more than 5 years, lower RHI values (P=0.08), EPC number (P=0.5), and higher PTH concentrations (P=0.09) than in patients with less than 1 year dialysis time were observed. No relationship between eNOS gene -786T>C, 894G>T, and 4a/4b polymorphisms and RHI, EPC, and CPC number was found.
  
  
  CONCLUSIONS
  This study shows an altered endothelial response, associated with reduced EPCs, and increased PTH in RTRs; the evaluation of endothelial status in RTRs may contribute to better assess the risk profile of these patients.
authors.affiliation: Department of Medical and Surgical Critical Care, Thrombosis Center, University of Florence, Azienda Ospedaliero-Universitaria Careggi, Florence, Italy. cinzia.fatini@unifi.it
authors.forename: Cinzia
authors.initials: C
authors.lastname: Fatini
authors.forename: Elena
authors.initials: E
authors.lastname: Sticchi
authors.forename: Francesca
authors.initials: F
authors.lastname: Cesari
authors.forename: Anna Maria
authors.initials: AM
authors.lastname: Gori
authors.forename: Gabriele
authors.initials: G
authors.lastname: Cioni
authors.forename: Margherita
authors.initials: M
authors.lastname: De Stefano
authors.forename: Elisabetta
authors.initials: E
authors.lastname: Bertoni
authors.forename: Nunzia
authors.initials: N
authors.lastname: Paudice
authors.forename: Maurizio
authors.initials: M
authors.lastname: Salvadori
authors.forename: Maria
authors.initials: M
authors.lastname: Zanazzi
authors.forename: Rosanna
authors.initials: R
authors.lastname: Abbate
mesh_terms: D000328:Adult; D000368:Aged; D001854:Bone Marrow Cells / Q000502:physiology*; D004730:Endothelium, Vascular / Q000503:physiopathology*; D005260:Female; D006801:Humans; D006940:Hyperemia / Q000503:physiopathology*; D016030:Kidney Transplantation / Q000473:pathology*; D008297:Male; D008875:Middle Aged; D052250:Nitric Oxide Synthase Type III / Q000235:genetics / Q000502:physiology; D010281:Parathyroid Hormone / Q000097:blood*; D011110:Polymorphism, Genetic; D013234:Stem Cells / Q000502:physiology*; D055815:Young Adult
chemical_list: D010281:Parathyroid Hormone; D052250:Nitric Oxide Synthase Type III